(Hypertension. 1995;25:1111-1115.)
© 1995 American Heart Association, Inc.
Articles |
A Noninvasive Computerized Tail-Cuff System for Measuring Blood Pressure in Mice
From the Departments of Pathology and Medicine, University of North Carolina at Chapel Hill.
Correspondence to Dr John H. Krege, 703 B.B.B., CB #7525, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599. E-mail krege@med.unc.edu.
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Abstract |
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Abstract We have validated a noninvasive computerized tail-cuff system for measuring blood pressure in mice. The system was designed to perform all functions automatically, including a programmable routine of cuff inflation and deflation, analysis and assignment of pulse rate and blood pressure, and recording of data electronically. To evaluate this system over a range of blood pressures, we gave groups of mice enalapril or NG-nitro-L-arginine methyl ester in their drinking water. For each of these groups, an equal number of control mice were given nothing in their drinking water. Tail-cuff blood pressures were recorded as the means of blood pressures determined on at least 3 days after at least 7 days of training. Tail-cuff enalapril and control group means were measured both 3 and 4 months after enalapril (or no drug) was begun; the group means at 3 months were not significantly different from the group means at 4 months. These results demonstrate that the system gives reproducible results. After the tail-cuff measurements were completed, intra-arterial blood pressures were attempted in all mice under unrestrained, unanesthetized conditions, and individual mouse (n=22) blood pressures with the use of the two methods were compared. The blood pressures from individual mice by tail-cuff and intra-arterial methods were highly correlated (r=.86, P<.01). The means for the four mouse groups were also highly correlated (r=.98, P<.02). These data show that blood pressures measured on trained mice by a computerized noninvasive tail-cuff system are reproducible and correlate well with intra-arterial blood pressures measured on unrestrained, unanesthetized mice.
Key Words: blood pressure determination, noninvasive • genetics • mice
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Introduction |
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The ability to measure noninvasively the blood pressure (BP) of genetically altered mice should advance efforts to elucidate the genetic determinants of hypertension. Although BP studies involving mice have been reported, we are unaware of previous validation of the tail-cuff method in unanesthetized mice.
Several valuable mouse models for the study of BP already exist. Using selective breeding strategies, Schlager1 derived the BP1 spontaneously hypertensive mouse strain, conclusively demonstrating that genetic factors are important determinants of BP in mice. Steinhelper et al2 used transgenic techniques to derive a mouse strain overexpressing atrial natriuretic peptide. The hypotensive phenotype demonstrated by the atrial natriuretic peptide transgenic mouse showed that greatly increased atrial natriuretic peptide expression can affect the tonic regulation of BP. Since the identification by Jeunemaitre and colleagues3 of the gene encoding angiotensinogen as a potential candidate gene in human hypertension, Smithies and Kim4 have reported the derivation (by gene targeting) of mice having increased and decreased copy numbers of the murine angiotensinogen gene. BP evaluation in these mice should directly test the effect of physiological increases and decreases in the expression of the angiotensinogen gene. These and other mouse strains will provide new means for the study of the complex etiology of hypertension.5 6 7 8 9 10 11 12 13 14 15
Direct intra-arterial assessment in unanesthetized, unrestrained animals is generally considered the most physiologically relevant means of BP determination.16 However, the technical difficulty of the surgery, the requirement for an invasive procedure, and the difficulty of maintaining catheter patency for long-term experiments are severe problems.17 Therefore, a noninvasive method of BP determination that correlates well with direct unanesthetized intra-arterial BP would be advantageous for the study of BP serially in mice at different ages or under varying environmental backgrounds.
Several investigators have reported excellent correlations between tail-cuff and intra-arterial BPs measured simultaneously in awake rats.18 19 These simultaneous direct comparisons of the methods have provided important validations of the tail-cuff system. However, because the conditions for these simultaneous measurements necessarily involve factors, including heating and restraint, that can affect BP,20 21 the relevance of tail-cuff data to normal resting physiology is often questioned.22 23 24
In this article, we demonstrate that BPs obtained by the described tail-cuff system during heating and restraint are reproducible and correlate strongly with subsequently measured intra-arterial BPs in the same mice not subjected to heating or restraint. This experimental design has the advantage that the tail-cuff and intra-arterial BP measurements are both performed under optimal conditions. Thus, the tail-cuff measurements are made in trained mice that have not undergone any invasive procedures, and the intra-arterial measurements are made without the stresses of heating and restraint required during the tail-cuff procedure.
The tail-cuff system to be described was designed and built by John E. Rogers and James P. Rogers (Visitech Systems, Inc, Apex, N.C.). Like the first tail-cuff approach,25 the system measures BP by determining the cuff pressure at which blood flow to the tail is eliminated. For the rapid and reproducible study of a large number of mice, the system evaluates the BPs of four mice at the same time using computer automation and analysis of all aspects of the tail-cuff procedure. It was hoped that such an automated approach would improve on already existing systems by increasing session-to-session reproducibility and by reducing investigator bias.
The system is housed in two boxes, allowing for the separation of mice undergoing BP evaluation from the vibration produced by the pressurizing pump. Four restraining units (3 cm wide, 3.3 cm high) are mounted on a surface maintained at 38°C. We found that placement of mice into the restraining units without prior preheating resulted in an adequate blood flow to the tail after approximately 3 to 5 minutes, as determined by a visually acceptable waveform amplitude on the computer monitor (waveform acquisition is described below).
Mouse tails are passed through a cuff (13 mm long, with a 9-mm diameter) and immobilized by adhesive tape in a V-shaped block between a light source above and a photoresistor below the tail. Evaluated photoelectrically, blood flow in the tails produces oscillating waveforms that are digitally sampled 200 times per second per channel. The waveforms, displayed in real time on a monitor, are computer analyzed before and during a programmable routine of cuff inflation and deflation. Programmable functions available by drop-down menu include (1) the number of waveforms analyzed to identify the amplitude and heart rate before each cuff inflation, (2) the number of preliminary unrecorded measurements, and (3) the number of recorded measurements per session. We describe under "Methods" our choices for these parameters. The software assigns BP values from a further set of programmable parameters. Tail-cuff BP is defined as the cuff inflation pressure at which the waveform amplitude falls below a programmable percentage, p, of its original amplitude for a specified number, n, of waveform cycles. Adjustment of these parameters allows BPs to be determined without interference from background noise. In Fig 1, we show a representative waveform and decay and illustrate a BP determination when p is 20% and n is 5—the values chosen for our present study. If the system is unable (before a cuff pressure of >200 mm Hg is reached) to identify a waveform decay (usually because of excessive movement of the mouse), the computer records "systolic time-out" for the measurement.
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The system records all data into comma-delimited computer files that can be loaded into a spreadsheet for analysis.
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Methods |
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Mice, Treatments, and Study Design
The mice were derived from crosses of strain 129xC57BL/6 and included 18 mice that were homozygous for a disruption of the apolipoprotein E gene26 and 8 wild-type mice. Male and female mice were 12 to 26 weeks old and weighed 20 to 35 g. Half of the apolipoprotein E mice received enalapril (30 mg/kg per day in drinking water, Merck Research Laboratories) and half received no drug. To assess the reproducibility of the tail-cuff system, we compared tail-cuff BPs measured at 3 and 4 months after enalapril (or no drug) was begun. Tail-cuff BPs of the wild-type mice were measured after half received NG-nitro-L-arginine methyl ester (20 mg/kg per day, Sigma Chemical Co) and half received no drug in their drinking water for 3 weeks. After the tail-cuff measurements were completed, intra-arterial BP assessment was attempted in all mice. The interval between tail-cuff and intra-arterial measurements averaged 9.3 days (range, 4 to 19 days). Tail-cuff BPs were compared with intra-arterial BPs for all mice in which the intra-arterial procedure was successful. Experiments were conducted in accordance with the guidelines for the care and use of animals approved by the University of North Carolina School of Medicine.
Tail-Cuff BP Measurements
In preliminary experiments, we found that the following
programmable settings, described above, gave reproducible BP
measurements. For (1), we found that analysis of 70 waveforms was
sufficient for the computer to determine heart rate and waveform
amplitude before each cuff inflation. For (2), 10 preliminary
unrecorded measurements were likewise sufficient for most mice to warm
up and give a waveform after placement into the machine. However, we
note that 7 days of training sessions (that is, sessions of unrecorded
measurements) were necessary for the mice to become accustomed to the
tail-cuff procedure as judged by the rapid appearance of a waveform
comparable to that in Fig 1. Sessions of recorded measurements were
then made by a single investigator (J.B.H.) from 1 to 5
PM daily on 3 to 5 consecutive days. For (3), each
session included 2 sets of 10 measurements, so that a total of 60 to
100 measurements was used for the determination of the BP of each
mouse. For inclusion of each set of measurements for an individual
mouse, we required that the computer successfully identify a BP (and
not "systolic time-out") in at least 6 of the 10 trials within
the set. The computer was able to do this in 283 of 286 (99%) sets of
measurements; the other 3 sets of measurements were discarded.
Intra-arterial BP Measurements
After completion of all tail-cuff measurements, intra-arterial
BPs were determined on the mouse groups described above. Surgeries were
performed in a uniform fashion by a single investigator (J.R.H.)
between 8 AM and noon. Mice were anesthetized with 0.03
mL of a 2:1 mixture of ketamine (100 mg/mL IM, Aveco Co) and xylazine
(20 mg/mL IM, Miles Inc) and placed on an operating surface maintained
at 38°C. A midline incision was made in the neck. With care taken to
avoid the vagus nerve and carotid sinus, the left carotid artery was
isolated below the level of the bifurcation and was tied off distally
with 5.0 silk suture, and a vascular clamp was applied proximally.
Approximately 3.5 mm of beveled Micro-Renanthane catheter tubing
(0.025-inch OD, 0.01-inch ID; Braintree Scientific) was inserted into
the vessel so that its tip was approximately at the junction of the
aorta and the carotid. The catheter was then firmly sutured in place.
The catheter, previously tunneled subcutaneously to exit at the nape of
the neck, was flushed with heparinized (20 U/mL) phosphate-buffered
saline, heat-sealed, and passed through and coiled into a flat,
button-shaped silicone elastomer pocket sewn to the skin between the
scapulae. When the mice appeared to have recovered from the effects of
anesthesia (from 3 to 5 PM, minimum of 4 hours after
completion of surgery), an open-bottomed box (12.7 cm long, 10.3 cm
wide, and 4.3 cm high, having a 7x1-cm slot in the roof for passage of
the catheter) was placed over each mouse in its own cage. The box was
carefully cleaned between mice to eliminate scents. The mice were free
to move but could not place tension on the catheters. Mice investigated
the box for varying lengths of time but were usually resting quietly
within about 10 minutes. BP waveforms from quietly resting mice were
obtained by a single investigator (J.H.K.) for about 10 minutes using
DTX transducers (Viggo Spectramed), PM1000 amplifiers (CWE, Inc), a DI
200 data-acquisition board, and Windaq data-acquisition and playback
software (Dataq Instruments). All waveforms from each mouse were
analyzed for peak, trough, and mean pressure (calculated as the
summation of all data points divided by the number of data points
obtained for the waveform), and rate with the use of ADVANCED
CODAS software (Dataq Instruments). For each mouse, the mean
arterial pressure and heart rate were defined as the average mean and
rate values for all waveforms obtained during the recording session.
Because we found in preliminary experiments that varying the sampling
rate of the computer system from 200 to 10 000 samples per second
altered the mean arterial pressures of three mice by 1 mm Hg or less,
all intra-arterial data were subsequently obtained with a sampling rate
of 200 samples per second per channel. Intra-arterial BPs were confined
to measurements on 1 day only because of reduced catheter
patency. Requirements for inclusion of data were a pulsatile waveform,
minimum heart rate of 400 beats per minute, and survival of the mouse
until the following day.
Data Analysis
Correlation coefficients were calculated in a standard fashion.
The probabilities of the observed correlations occurring by chance were
from Table V.A. in Fisher.27 Mean arterial BP and
tail-cuff BP for individual mice were analyzed using a model II
regression analysis.28 In this type of analysis,
it is assumed that there is "error" in both the tail-cuff and
intra-arterial readings so that two regressions are performed: the
regression of tail-cuff BP on intra-arterial BP and the regression of
intra-arterial BP on tail-cuff BP. For both regressions, the slope and
intercept are reported, with intra-arterial BP as the x
variable and tail-cuff BP as the y variable.
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Results |
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Surgical Outcomes
Table 1 presents surgical outcomes from the catheterization procedure. We successfully acquired intra-arterial BP data in 81% of mice that had already undergone tail-cuff BP determination.
Reproducibility of the Tail-Cuff System
The mean (±SEM) tail-cuff pressure of the enalapril group (n=9)
was 103.8±5.5 mm Hg after 3 months and 102.6±2.6 mm Hg after 4
months of drug treatment. There was no significant difference in these
measurements (P=.85 by paired two-sample t test
for means). The control group (n=9) had a mean tail-cuff pressure of
119.8±4.0 mm Hg after 3 months and 122.8±1.8 mm Hg after 4 months
of receiving no drug in their drinking water. Again, there was no
significant difference in these measurements (P=.32). Thus,
the tail-cuff system gives reproducible results.
Comparison of Tail-Cuff and Intra-arterial Pressures
Fig 2 compares tail-cuff BPs with resting arterial
BPs. Data points are shown for each individual mouse and for the four
group means. Clearly, in these 22 trained mice, there is a strong
correlation between the two methods of BP measurement
(r=.86, P<.01). The regression of tail-cuff BP
on intra-arterial BP revealed a slope (±SEM) of 0.79±0.10 and an
intercept of 30. The reverse regression of intra-arterial BP on
tail-cuff BP revealed a slope of 1.1±0.14 and an intercept of 1.46.
The means for the four mouse groups, presented in Table 2, were also highly correlated (r=.98,
P<.02).
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Comparison of Tail-Cuff and Intra-arterial Heart Rates
The mean heart rates for the three mouse groups measured by
intra-arterial and tail-cuff methods are presented in Table 2.
Heart rates for all groups were lower in mice during intra-arterial
monitoring than during tail-cuff monitoring (P<.05 for all
comparisons). A comparison of the heart rates of either treatment group
with its corresponding control group showed no significant differences
by either tail-cuff or intra-arterial monitoring (P>.2 for
all comparisons).
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Discussion |
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Our study describes a noninvasive computer-automated tail-cuff system and confirms that tail-cuff BPs obtained in trained mice are reproducible and correlate well with intra-arterial BPs measured in the same mice in the resting state. Because we could not be sure we had eliminated damping from our intra-arterial measurements, we did not compare systolic pressures by the two methods. Therefore, the finding that group mean tail-cuff (systolic) BPs were from 1 to 9 mm Hg higher than mean arterial BPs may simply reflect the difference between systolic and mean BPs. Alternatively, the stresses of restraint and heating during tail-cuff measurements or the stress of surgery before intra-arterial measurements may account for the differences.
Individual tail-cuff measurements are subject to variability because of the varied response of individual animals to the stresses (heating and restraint) involved in the procedure. To reduce the effect of this variability, we took many measurements. The tail-cuff data presented for each mouse reflect the means of 60 to 100 tail-cuff measurements (20 measurements per day for 3 to 5 days). The use of a computer to analyze the waveforms during the tail-cuff procedure facilitated the acquisition of this many measurements from each mouse by eliminating the need for time-consuming evaluation of strip-chart tracings by hand.
The heart rate differences between the two methods are notable. The systematically higher heart rates in mice when evaluated by the tail-cuff method might reflect a stress response to restraint and heating and/or might reflect residual heart rate–lowering effects of anesthesia in the intra-arterial group. Of relevance is our observation that the tail-cuff heart rates in an untrained group of mice were significantly increased compared with heart rates in the trained group of mice (711±4.8 compared with 698±3.6 beats per minute, P<.05), suggesting that heart rate decreases with training and thus presumably with reduction in stress. Our intra-arterial heart rates are much higher than those reported by Milano et al5 in anesthetized mice (340±20 beats per minute); they are similar to those reported by Kurihara et al6 in unanesthetized mice on the day after surgery (590±12 beats per minute) but lower than those reported by Steinhelper et al2 on the day after surgery (704±16 beats per minute).
In conclusion, we have shown that tail-cuff measurements in trained mice are reproducible and correlate well with mean arterial pressures in unrestrained, unanesthetized mice. Thus, the described noninvasive tail-cuff system for mice is likely to be valuable for studies in which a noninvasive approach is desired and for long-term experiments such as those involving various drug treatments or diets.
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Acknowledgments |
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This research was supported by grant HL-49277 from the National Heart, Lung, and Blood Institute. John Krege is a Howard Hughes Medical Institute Physician Postdoctoral Fellow. The authors thank Chris Best, Thomas Coffman, Jenny Lynch, and Edward Shesely for their advice and help.
Received August 23, 1994; first decision October 19, 1994; accepted January 13, 1995.
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K. Tsukuda, M. Mogi, J.-M. Li, J. Iwanami, L.-J. Min, A. Sakata, T. Fujita, M. Iwai, and M. Horiuchi Diabetes-Associated Cognitive Impairment Is Improved by a Calcium Channel Blocker, Nifedipine Hypertension, February 1, 2008; 51(2): 528 - 533. [Abstract] [Full Text] [PDF]
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K. Tsukuda, M. Mogi, J.-M. Li, J. Iwanami, L.-J. Min, A. Sakata, T. Fujita, M. Iwai, and M. Horiuchi Amelioration of Cognitive Impairment in the Type-2 Diabetic Mouse by the Angiotensin II Type-1 Receptor Blocker Candesartan Hypertension, December 1, 2007; 50(6): 1099 - 1105. [Abstract] [Full Text] [PDF]
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J. Xu, O. A. Carretero, C.-X. Lin, M. A. Cavasin, E. G. Shesely, J. J. Yang, T. L. Reudelhuber, and X.-P. Yang Role of cardiac overexpression of ANG II in the regulation of cardiac function and remodeling postmyocardial infarction Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1900 - H1907. [Abstract] [Full Text] [PDF]
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N. K. LeBrasseur, T.-A. S. Duhaney, D. S. De Silva, L. Cui, P. C. Ip, L. Joseph, and F. Sam Effects of Fenofibrate on Cardiac Remodeling in Aldosterone-Induced Hypertension Hypertension, September 1, 2007; 50(3): 489 - 496. [Abstract] [Full Text] [PDF]
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D. Zhao, E. Vellaichamy, N. K. Somanna, and K. N. Pandey Guanylyl cyclase/natriuretic peptide receptor-A gene disruption causes increased adrenal angiotensin II and aldosterone levels Am J Physiol Renal Physiol, July 1, 2007; 293(1): F121 - F127. [Abstract] [Full Text] [PDF]
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R. Dackor, K. Fritz-Six, O. Smithies, and K. Caron Receptor Activity-modifying Proteins 2 and 3 Have Distinct Physiological Functions from Embryogenesis to Old Age J. Biol. Chem., June 22, 2007; 282(25): 18094 - 18099. [Abstract] [Full Text] [PDF]
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C. K. Fujihara, D. M. A. C. Malheiros, and R. Zatz Losartan-hydrochlorothiazide association promotes lasting blood pressure normalization and completely arrests long-term renal injury in the 5/6 ablation model Am J Physiol Renal Physiol, June 1, 2007; 292(6): F1810 - F1818. [Abstract] [Full Text] [PDF]
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 M. Kakoki, R. W. McGarrah, H.-S. Kim, and O. Smithies Bradykinin B1 and B2 receptors both have protective roles in renal ischemia/reperfusion injury PNAS, May 1, 2007; 104(18): 7576 - 7581. [Abstract] [Full Text] [PDF]
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T.-A. S. Duhaney, L. Cui, M. K. Rude, N. K. Lebrasseur, S. Ngoy, D. S. De Silva, D. A. Siwik, R. Liao, and F. Sam Peroxisome Proliferator-Activated Receptor {alpha}-Independent Actions of Fenofibrate Exacerbates Left Ventricular Dilation and Fibrosis in Chronic Pressure Overload Hypertension, May 1, 2007; 49(5): 1084 - 1094. [Abstract] [Full Text] [PDF]
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 E. Stoyanova, M. Trudel, H. Felfly, D. Garcia, and G. Cloutier Characterization of circulatory disorders in {beta}-thalassemic mice by noninvasive ultrasound biomicroscopy Physiol Genomics, March 14, 2007; 29(1): 84 - 90. [Abstract] [Full Text] [PDF]
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K. Caron, J. Hagaman, T. Nishikimi, H.-S. Kim, and O. Smithies Adrenomedullin gene expression differences in mice do not affect blood pressure but modulate hypertension-induced pathology in males PNAS, February 27, 2007; 104(9): 3420 - 3425. [Abstract] [Full Text] [PDF]
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 M.-Y. Chang, E. Parker, M. El Nahas, J. L. Haylor, and A. C.M. Ong Endothelin B Receptor Blockade Accelerates Disease Progression in a Murine Model of Autosomal Dominant Polycystic Kidney Disease J. Am. Soc. Nephrol., February 1, 2007; 18(2): 560 - 569. [Abstract] [Full Text] [PDF]
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 X. Hua, M. Kovarova, K. D. Chason, M. Nguyen, B. H. Koller, and S. L. Tilley Enhanced mast cell activation in mice deficient in the A2b adenosine receptor J. Exp. Med., January 22, 2007; 204(1): 117 - 128. [Abstract] [Full Text] [PDF]
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S. P. Kessler, P. deS. Senanayake, C. Gaughan, and G. C. Sen Vascular expression of germinal ACE fails to maintain normal blood pressure in ACE-/- mice FASEB J, January 1, 2007; 21(1): 156 - 166. [Abstract] [Full Text] [PDF]
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R. Ramchandran, T. Takezako, Y. Saad, L. Stull, B. Fink, H. Yamada, S. Dikalov, D. G. Harrison, C. Moravec, and S. S. Karnik Angiotensinergic stimulation of vascular endothelium in mice causes hypotension, bradycardia, and attenuated angiotensin response PNAS, December 12, 2006; 103(50): 19087 - 19092. [Abstract] [Full Text] [PDF]
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N. Makhanova, M. L.S. Sequeira-Lopez, R. A. Gomez, H.-S. Kim, and O. Smithies Disturbed Homeostasis in Sodium-Restricted Mice Heterozygous and Homozygous for Aldosterone Synthase Gene Disruption Hypertension, December 1, 2006; 48(6): 1151 - 1159. [Abstract] [Full Text] [PDF]
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D. Chansel, M. Ciroldi, S. Vandermeersch, L. F Jackson, A.-M. Gomez, D. Henrion, D. C. Lee, T. M. Coffman, S. Richard, J.-C. Dussaule, et al. Heparin binding EGF is necessary for vasospastic response to endothelin FASEB J, September 1, 2006; 20(11): 1936 - 1938. [Abstract] [Full Text] [PDF]
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S. Miriyala, M. C. Gongora Nieto, C. Mingone, D. Smith, S. Dikalov, D. G. Harrison, and H. Jo Bone Morphogenic Protein-4 Induces Hypertension in Mice: Role of Noggin, Vascular NADPH Oxidases, and Impaired Vasorelaxation Circulation, June 20, 2006; 113(24): 2818 - 2825. [Abstract] [Full Text] [PDF]
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 A. R. Karuri, Y. Huang, S. Bodreddigari, C. H. Sutter, B. D. Roebuck, T. W. Kensler, and T. R. Sutter 3H-1,2-Dithiole-3-thione Targets Nuclear Factor {kappa}B to Block Expression of Inducible Nitric-Oxide Synthase, Prevents Hypotension, and Improves Survival in Endotoxemic Rats J. Pharmacol. Exp. Ther., April 1, 2006; 317(1): 61 - 67. [Abstract] [Full Text] [PDF]
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H. Matsusaka, T. Ide, S. Matsushima, M. Ikeuchi, T. Kubota, K. Sunagawa, S. Kinugawa, and H. Tsutsui Targeted Deletion of Matrix Metalloproteinase 2 Ameliorates Myocardial Remodeling in Mice With Chronic Pressure Overload Hypertension, April 1, 2006; 47(4): 711 - 717. [Abstract] [Full Text] [PDF]
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W. Ye, H. Zhang, E. Hillas, D. E. Kohan, R. L. Miller, R. D. Nelson, M. Honeggar, and T. Yang Expression and function of COX isoforms in renal medulla: evidence for regulation of salt sensitivity and blood pressure Am J Physiol Renal Physiol, February 1, 2006; 290(2): F542 - F549. [Abstract] [Full Text] [PDF]
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N. Makhanova, G. Lee, N. Takahashi, M. L. Sequeira Lopez, R. A. Gomez, H.-S. Kim, and O. Smithies Kidney function in mice lacking aldosterone Am J Physiol Renal Physiol, January 1, 2006; 290(1): F61 - F69. [Abstract] [Full Text] [PDF]
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S. B. Gurley, S. E. Clare, K. P. Snow, A. Hu, T. W. Meyer, and T. M. Coffman Impact of genetic background on nephropathy in diabetic mice Am J Physiol Renal Physiol, January 1, 2006; 290(1): F214 - F222. [Abstract] [Full Text] [PDF]
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Y.-H. Liu, O. A. Carretero, O. H. Cingolani, T.-D. Liao, Y. Sun, J. Xu, L. Y. Li, P. J. Pagano, J. J. Yang, and X.-P. Yang Role of inducible nitric oxide synthase in cardiac function and remodeling in mice with heart failure due to myocardial infarction Am J Physiol Heart Circ Physiol, December 1, 2005; 289(6): H2616 - H2623. [Abstract] [Full Text] [PDF]
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 D. Predescu, S. Predescu, J. Shimizu, K. Miyawaki-Shimizu, and A. B. Malik Constitutive eNOS-derived nitric oxide is a determinant of endothelial junctional integrity Am J Physiol Lung Cell Mol Physiol, September 1, 2005; 289(3): L371 - L381. [Abstract] [Full Text] [PDF]
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K. R. Schmelzer, L. Kubala, J. W. Newman, I.-H. Kim, J. P. Eiserich, and B. D. Hammock Soluble epoxide hydrolase is a therapeutic target for acute inflammation PNAS, July 12, 2005; 102(28): 9772 - 9777. [Abstract] [Full Text] [PDF]
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 G. Lee, N. Makhanova, K. Caron, M. L. S. Lopez, R. A. Gomez, O. Smithies, and H.-S. Kim Homeostatic Responses in the Adrenal Cortex to the Absence of Aldosterone in Mice Endocrinology, June 1, 2005; 146(6): 2650 - 2656. [Abstract] [Full Text] [PDF]
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T. Yang, Y. G. Huang, W. Ye, P. Hansen, J. B. Schnermann, and J. P. Briggs Influence of genetic background and gender on hypertension and renal failure in COX-2-deficient mice Am J Physiol Renal Physiol, June 1, 2005; 288(6): F1125 - F1132. [Abstract] [Full Text] [PDF]
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B. D. Freedman, E.-J. Lee, Y. Park, and J. L. Jameson A Dominant Negative Peroxisome Proliferator-activated Receptor-{gamma} Knock-in Mouse Exhibits Features of the Metabolic Syndrome J. Biol. Chem., April 29, 2005; 280(17): 17118 - 17125. [Abstract] [Full Text] [PDF]
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T. Nishikimi, J. R. Hagaman, N. Takahashi, H.-S. Kim, H. Matsuoka, O. Smithies, and N. Maeda Increased susceptibility to heart failure in response to volume overload in mice lacking natriuretic peptide receptor-A gene Cardiovasc Res, April 1, 2005; 66(1): 94 - 103. [Abstract] [Full Text] [PDF]
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L.-G. Jia, C. Donnet, R. C. Bogaev, R. J. Blatt, C. E. McKinney, K. H. Day, S. S. Berr, L. R. Jones, J. R. Moorman, K. J. Sweadner, et al. Hypertrophy, increased ejection fraction, and reduced Na-K-ATPase activity in phospholemman-deficient mice Am J Physiol Heart Circ Physiol, April 1, 2005; 288(4): H1982 - H1988. [Abstract] [Full Text] [PDF]
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J. Xu, O. A. Carretero, Y. Sun, E. G. Shesely, N.-E. Rhaleb, Y.-H. Liu, T.-D. Liao, J. J. Yang, M. Bader, and X.-P. Yang Role of the B1 Kinin Receptor in the Regulation of Cardiac Function and Remodeling After Myocardial Infarction Hypertension, April 1, 2005; 45(4): 747 - 753. [Abstract] [Full Text] [PDF]
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 T. W. Kurtz, K. A. Griffin, A. K. Bidani, R. L. Davisson, and J. E. Hall Recommendations for Blood Pressure Measurement in Humans and Experimental Animals: Part 2: Blood Pressure Measurement in Experimental Animals. A Statement for Professionals From the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research Arterioscler. Thromb. Vasc. Biol., March 1, 2005; 25(3): e22 - e33. [Abstract] [Full Text] [PDF]
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K. E. Bernstein, H. D. Xiao, J. W. Adams, K. Frenzel, P. Li, X. Z. Shen, J. M. Cole, and S. Fuchs Establishing the Role of Angiotensin-Converting Enzyme in Renal Function and Blood Pressure Control through the Analysis of Genetically Modified Mice J. Am. Soc. Nephrol., March 1, 2005; 16(3): 583 - 591. [Full Text] [PDF]
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 C. F. Benjamim, C. Canetti, F. Q. Cunha, S. L. Kunkel, and M. Peters-Golden Opposing and Hierarchical Roles of Leukotrienes in Local Innate Immune versus Vascular Responses in a Model of Sepsis J. Immunol., February 1, 2005; 174(3): 1616 - 1620. [Abstract] [Full Text] [PDF]
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M. Lassila, K. Jandeleit-Dahm, K. K. Seah, C. M. Smith, A. C. Calkin, T. J. Allen, and M. E. Cooper Imatinib Attenuates Diabetic Nephropathy in Apolipoprotein E-Knockout Mice J. Am. Soc. Nephrol., February 1, 2005; 16(2): 363 - 373. [Abstract] [Full Text] [PDF]
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G. M. Kuster, E. Kotlyar, M. K. Rude, D. A. Siwik, R. Liao, W. S. Colucci, and F. Sam Mineralocorticoid Receptor Inhibition Ameliorates the Transition to Myocardial Failure and Decreases Oxidative Stress and Inflammation in Mice With Chronic Pressure Overload Circulation, February 1, 2005; 111(4): 420 - 427. [Abstract] [Full Text] [PDF]
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T. W. Kurtz, K. A. Griffin, A. K. Bidani, R. L. Davisson, and J. E. Hall Recommendations for Blood Pressure Measurement in Humans and Experimental Animals: Part 2: Blood Pressure Measurement in Experimental Animals: A Statement for Professionals From the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research Hypertension, February 1, 2005; 45(2): 299 - 310. [Abstract] [Full Text] [PDF]
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K. M. I. Caron, L. R. James, G. Lee, H.-S. Kim, and O. Smithies Lifelong genetic minipumps Physiol Genomics, January 20, 2005; 20(2): 203 - 209. [Abstract] [Full Text] [PDF]
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 S. Copeland, H. S. Warren, S. F. Lowry, S. E. Calvano, D. Remick, and the Inflammation and the Host Response to Injury I Acute Inflammatory Response to Endotoxin in Mice and Humans Clin. Vaccine Immunol., January 1, 2005; 12(1): 60 - 67. [Abstract] [Full Text] [PDF]
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N. Takahashi, M. L. S. S. Lopez, J. E. Cowhig Jr., M. A. Taylor, T. Hatada, E. Riggs, G. Lee, R. A. Gomez, H.-S. Kim, and O. Smithies Ren1c Homozygous Null Mice Are Hypotensive and Polyuric, but Heterozygotes Are Indistinguishable from Wild-Type J. Am. Soc. Nephrol., January 1, 2005; 16(1): 125 - 132. [Abstract] [Full Text] [PDF]
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A. Benigni, D. Corna, C. Zoja, L. Longaretti, E. Gagliardini, N. Perico, T. M. Coffman, and G. Remuzzi Targeted Deletion of Angiotensin II Type 1A Receptor Does not Protect Mice from Progressive Nephropathy of Overload Proteinuria J. Am. Soc. Nephrol., October 1, 2004; 15(10): 2666 - 2674. [Abstract] [Full Text] [PDF]
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 B. A. Pederson, H. Chen, J. M. Schroeder, W. Shou, A. A. DePaoli-Roach, and P. J. Roach Abnormal Cardiac Development in the Absence of Heart Glycogen Mol. Cell. Biol., August 15, 2004; 24(16): 7179 - 7187. [Abstract] [Full Text] [PDF]
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T. H. Le, M. I. Oliverio, H.-S. Kim, H. Salzler, R. C. Dash, D. N. Howell, O. Smithies, S. Bronson, and T. M. Coffman A {gamma}GT-AT1A receptor transgene protects renal cortical structure in AT1 receptor-deficient mice Physiol Genomics, August 11, 2004; 18(3): 290 - 298. [Abstract] [Full Text] [PDF]
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M. Lassila, K. K. Seah, T. J. Allen, V. Thallas, M. C. Thomas, R. Candido, W. C. Burns, J. M. Forbes, A. C. Calkin, M. E. Cooper, et al. Accelerated Nephropathy in Diabetic Apolipoprotein E-Knockout Mouse: Role of Advanced Glycation End Products J. Am. Soc. Nephrol., August 1, 2004; 15(8): 2125 - 2138. [Abstract] [Full Text] [PDF]
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 C. F. Deschepper, J. L. Olson, M. Otis, and N. Gallo-Payet Characterization of blood pressure and morphological traits in cardiovascular-related organs in 13 different inbred mouse strains J Appl Physiol, July 1, 2004; 97(1): 369 - 376. [Abstract] [Full Text] [PDF]
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 J. M. Forbes, L. T. L. Yee, V. Thallas, M. Lassila, R. Candido, K. A. Jandeleit-Dahm, M. C. Thomas, W. C. Burns, E. K. Deemer, S. R. Thorpe, et al. Advanced Glycation End Product Interventions Reduce Diabetes-Accelerated Atherosclerosis Diabetes, July 1, 2004; 53(7): 1813 - 1823. [Abstract] [Full Text] [PDF]
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S. E. Whitesall, J. B. Hoff, A. P. Vollmer, and L. G. D'Alecy Comparison of simultaneous measurement of mouse systolic arterial blood pressure by radiotelemetry and tail-cuff methods Am J Physiol Heart Circ Physiol, June 1, 2004; 286(6): H2408 - H2415. [Abstract] [Full Text] [PDF]
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M. Lassila, T. J. Allen, Z. Cao, V. Thallas, K. A. Jandeleit-Dahm, R. Candido, and M. E. Cooper Imatinib Attenuates Diabetes-Associated Atherosclerosis Arterioscler. Thromb. Vasc. Biol., May 1, 2004; 24(5): 935 - 942. [Abstract] [Full Text]
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S. Fuchs, H. D. Xiao, J. M. Cole, J. W. Adams, K. Frenzel, A. Michaud, H. Zhao, G. Keshelava, M. R. Capecchi, P. Corvol, et al. Role of the N-terminal Catalytic Domain of Angiotensin-converting Enzyme Investigated by Targeted Inactivation in Mice J. Biol. Chem., April 16, 2004; 279(16): 15946 - 15953. [Abstract] [Full Text] [PDF]
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K. M. I. Caron, L. R. James, H.-S. Kim, J. Knowles, R. Uhlir, L. Mao, J. R. Hagaman, W. Cascio, H. Rockman, and O. Smithies Cardiac hypertrophy and sudden death in mice with a genetically clamped renin transgene PNAS, March 2, 2004; 101(9): 3106 - 3111. [Abstract] [Full Text] [PDF]
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A. Paul, K. W.S. Ko, L. Li, V. Yechoor, M. A. McCrory, A. J. Szalai, and L. Chan C-Reactive Protein Accelerates the Progression of Atherosclerosis in Apolipoprotein E-Deficient Mice Circulation, February 10, 2004; 109(5): 647 - 655. [Abstract] [Full Text] [PDF]
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T. H. Le, A. B. Fogo, H. R. Salzler, T. Vinogradova, M. I. Oliverio, D. A. Marchuk, and T. M. Coffman Modifier Locus on Mouse Chromosome 3 for Renal Vascular Pathology in AT1A Receptor-Deficiency Hypertension, February 1, 2004; 43(2): 445 - 451. [Abstract] [Full Text] [PDF]
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 B. Moreno-Lopez, C. Romero-Grimaldi, J. A. Noval, M. Murillo-Carretero, E. R. Matarredona, and C. Estrada Nitric Oxide Is a Physiological Inhibitor of Neurogenesis in the Adult Mouse Subventricular Zone and Olfactory Bulb J. Neurosci., January 7, 2004; 24(1): 85 - 95. [Abstract] [Full Text] [PDF]
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H. Dayoub, V. Achan, S. Adimoolam, J. Jacobi, M. C. Stuehlinger, B.-y. Wang, P. S. Tsao, M. Kimoto, P. Vallance, A. J. Patterson, et al. Dimethylarginine Dimethylaminohydrolase Regulates Nitric Oxide Synthesis: Genetic and Physiological Evidence Circulation, December 16, 2003; 108(24): 3042 - 3047. [Abstract] [Full Text] [PDF]
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A. Zahabi, S. Picard, N. Fortin, T. L. Reudelhuber, and C. F. Deschepper Expression of Constitutively Active Guanylate Cyclase in Cardiomyocytes Inhibits the Hypertrophic Effects of Isoproterenol and Aortic Constriction on Mouse Hearts J. Biol. Chem., November 28, 2003; 278(48): 47694 - 47699. [Abstract] [Full Text] [PDF]
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D. D. L. Woo and I. Kurtz Mapping blood pressure loci in (A/J x B6)F2 mice Physiol Genomics, November 11, 2003; 15(3): 236 - 242. [Abstract] [Full Text] [PDF]
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K. Kazama, G. Wang, K. Frys, J. Anrather, and C. Iadecola Angiotensin II attenuates functional hyperemia in the mouse somatosensory cortex Am J Physiol Heart Circ Physiol, November 1, 2003; 285(5): H1890 - H1899. [Abstract] [Full Text] [PDF]
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S. Bro, J. F. Bentzon, E. Falk, C. B. Andersen, K. Olgaard, and L. B. Nielsen Chronic Renal Failure Accelerates Atherogenesis in Apolipoprotein E-Deficient Mice J. Am. Soc. Nephrol., October 1, 2003; 14(10): 2466 - 2474. [Abstract] [Full Text] [PDF]
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T. H. Le, H.-S. Kim, A. M. Allen, R. F. Spurney, O. Smithies, and T. M. Coffman Physiological Impact of Increased Expression of the AT1 Angiotensin Receptor Hypertension, October 1, 2003; 42(4): 507 - 514. [Abstract] [Full Text] [PDF]
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M. S. Taylor, A. D. Bonev, T. P. Gross, D. M. Eckman, J. E. Brayden, C. T. Bond, J. P. Adelman, and M. T. Nelson Altered Expression of Small-Conductance Ca2+-Activated K+ (SK3) Channels Modulates Arterial Tone and Blood Pressure Circ. Res., July 25, 2003; 93(2): 124 - 131. [Abstract] [Full Text] [PDF]
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C. R. Hampton, A. Shimamoto, C. L. Rothnie, J. Griscavage-Ennis, A. Chong, D. J. Dix, E. D. Verrier, and T. H. Pohlman HSP70.1 and -70.3 are required for late-phase protection induced by ischemic preconditioning of mouse hearts Am J Physiol Heart Circ Physiol, July 11, 2003; 285(2): H866 - H874. [Abstract] [Full Text] [PDF]
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N. Takahashi, J. R. Hagaman, H.-S. Kim, and O. Smithies Minireview: Computer Simulations of Blood Pressure Regulation by the Renin-Angiotensin System Endocrinology, June 1, 2003; 144(6): 2184 - 2190. [Abstract] [Full Text] [PDF]
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M. R. Alexander, J. W. Knowles, T. Nishikimi, and N. Maeda Increased Atherosclerosis and Smooth Muscle Cell Hypertrophy in Natriuretic Peptide Receptor A-/-Apolipoprotein E-/- Mice Arterioscler. Thromb. Vasc. Biol., June 1, 2003; 23(6): 1077 - 1082. [Abstract] [Full Text] [PDF]
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S. P. Kessler, P. deS. Senanayake, T. S. Scheidemantel, J. B. Gomos, T. M. Rowe, and G. C. Sen Maintenance of Normal Blood Pressure and Renal Functions Are Independent Effects of Angiotensin-converting Enzyme J. Biol. Chem., May 30, 2003; 278(23): 21105 - 21112. [Abstract] [Full Text] [PDF]
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K. Kramer and L. B. Kinter Evaluation and applications of radiotelemetry in small laboratory animals Physiol Genomics, May 13, 2003; 13(3): 197 - 205. [Abstract] [Full Text] [PDF]
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K. L. Svenson, M. A. Bogue, and L. L. Peters Genetic Models in Applied Physiology: Invited Review: Identifying new mouse models of cardiovascular disease: a review of high-throughput screens of mutagenized and inbred strains J Appl Physiol, April 1, 2003; 94(4): 1650 - 1659. [Abstract] [Full Text] [PDF]
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V. Gross and F. C. Luft Exercising Restraint in Measuring Blood Pressure in Conscious Mice Hypertension, April 1, 2003; 41(4): 879 - 881. [Full Text] [PDF]
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J. M. Cole, N. Khokhlova, R. L. Sutliff, J. W. Adams, K. M. Disher, H. Zhao, M. R. Capecchi, P. Corvol, and K. E. Bernstein Mice Lacking Endothelial ACE: Normal Blood Pressure With Elevated Angiotensin II Hypertension, February 1, 2003; 41(2): 313 - 321. [Abstract] [Full Text] [PDF]
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N. Lochard, D. W. Silversides, J. P. van Kats, C. Mercure, and T. L. Reudelhuber Brain-specific Restoration of Angiotensin II Corrects Renal Defects Seen in Angiotensinogen-deficient Mice J. Biol. Chem., January 17, 2003; 278(4): 2184 - 2189. [Abstract] [Full Text] [PDF]
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J. W. Meyer, M. Flagella, R. L. Sutliff, J. N. Lorenz, M. L. Nieman, C. S. Weber, R. J. Paul, and G. E. Shull Decreased blood pressure and vascular smooth muscle tone in mice lacking basolateral Na+-K+-2Cl- cotransporter Am J Physiol Heart Circ Physiol, November 1, 2002; 283(5): H1846 - H1855. [Abstract] [Full Text] [PDF]
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S. P. Didion, M. J. Ryan, G. L. Baumbach, C. D. Sigmund, and F. M. Faraci Superoxide contributes to vascular dysfunction in mice that express human renin and angiotensinogen Am J Physiol Heart Circ Physiol, October 1, 2002; 283(4): H1569 - H1576. [Abstract] [Full Text] [PDF]
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U. Landmesser, H. Cai, S. Dikalov, L. McCann, J. Hwang, H. Jo, S. M. Holland, and D. G. Harrison Role of p47phox in Vascular Oxidative Stress and Hypertension Caused by Angiotensin II Hypertension, October 1, 2002; 40(4): 511 - 515. [Abstract] [Full Text] [PDF]
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A. J. Mangrum, R. A. Gomez, and V. F. Norwood Effects of AT1A receptor deletion on blood pressure and sodium excretion during altered dietary salt intake Am J Physiol Renal Physiol, September 1, 2002; 283(3): F447 - F453. [Abstract] [Full Text] [PDF]
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F. Sugiyama, G. A. Churchill, R. Li, L. J. M. Libby, T. Carver, K.-I. Yagami, S. W. M. John, and B. Paigen QTL associated with blood pressure, heart rate, and heart weight in CBA/CaJ and BALB/cJ mice Physiol Genomics, July 12, 2002; 10(1): 5 - 12. [Abstract] [Full Text] [PDF]
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R. Candido, K. A. Jandeleit-Dahm, Z. Cao, S. P. Nesteroff;, W. C. Burns, S. M. Twigg, R. J. Dilley, M. E. Cooper, and T. J. Allen Prevention of Accelerated Atherosclerosis by Angiotensin-Converting Enzyme Inhibition in Diabetic Apolipoprotein E-Deficient Mice Circulation, July 9, 2002; 106(2): 246 - 253. [Abstract] [Full Text] [PDF]
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K. M. I. Caron, L. R. James, H.-S. Kim, S. G. Morham, M. L. S. S. Lopez, R. A. Gomez, T. L. Reudelhuber, and O. Smithies A genetically clamped renin transgene for the induction of hypertension PNAS, June 11, 2002; 99(12): 8248 - 8252. [Abstract] [Full Text] [PDF]
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B. J. A. Janssen and J. F. M. Smits Autonomic control of blood pressure in mice: basic physiology and effects of genetic modification Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2002; 282(6): R1545 - R1564. [Abstract] [Full Text] [PDF]
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J. N. Lorenz A practical guide to evaluating cardiovascular, renal, and pulmonary function in mice Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2002; 282(6): R1565 - R1582. [Abstract] [Full Text] [PDF]
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N. Takahashi, H. L. Brooks, J. B. Wade, W. Liu, Y. Kondo, S. Ito, M. A. Knepper, and O. Smithies Posttranscriptional Compensation for Heterozygous Disruption of the Kidney-Specific NaK2Cl Cotransporter Gene J. Am. Soc. Nephrol., March 1, 2002; 13(3): 604 - 610. [Abstract] [Full Text] [PDF]
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A. Y. H. Wong, S. Kulandavelu, K. J. Whiteley, D. Qu, B. L. Langille, and S. L. Adamson Maternal cardiovascular changes during pregnancy and postpartum in mice Am J Physiol Heart Circ Physiol, March 1, 2002; 282(3): H918 - H925. [Abstract] [Full Text] [PDF]
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 M. W Manning, L. A Cassis, J. Huang, S. J Szilvassy, and A. Daugherty Abdominal aortic aneurysms: fresh insights from a novel animal model of the disease Vascular Medicine, February 1, 2002; 7(1): 45 - 54. [Abstract] [PDF]
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