(Hypertension. 1996;27:760-765.)
© 1996 American Heart Association, Inc.
Articles |
Opposing Actions of Angiotensin II on Microvascular Growth and Arterial Blood Pressure
From the Department of Physiology, Medical College of Wisconsin, Milwaukee.
Correspondence to Andrew S. Greene, PhD, Department of Physiology, Medical College of Wisconsin, 8701 Watertown Plank Rd, Milwaukee, WI 53226. E-mail agreene@mcw.edu.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Abstract We performed studies to further elucidate the mechanisms of angiotensin II (Ang II)–induced angiogenesis of the microvasculature. Rats were placed on a high salt diet (4% NaCl), and Ang II was infused at a subpressor rate (5 ng/kg per minute) for 3 days. Blood pressure was measured daily for 2 control and 3 infusion days. Microvessel density in the cremaster muscle was measured at the end of the infusion. Vessel density in rats that received subpressor Ang II infusion increased by 12.6% compared with rats that received vehicle infusion. When the angiotensin type 2 (AT2) receptor antagonist PD 123319 was coinfused with Ang II, blood pressure was elevated and vessel density increased above that observed with Ang II infusion alone (23% increase). When the AT1 receptor antagonist losartan was coinfused with Ang II, blood pressure was lower than control and vessel density was reduced compared with the Ang II group but was still greater than control (7.8% increase). In this study, Ang II stimulated angiogenesis in the rat cremaster muscle; this effect was enhanced by AT2 antagonism and inhibited by AT1 antagonism. Ang II infusion at a subpressor dose resulted in a pressor response with AT2 antagonism and a depressor response with AT1 antagonism. This suggests that in the microvasculature, the AT1 receptor mediates angiogenesis and vasoconstriction, and the AT2 receptor mediates an inhibition of angiogenesis and vasodilation.
Key Words: receptors, angiotensin • angiotensin • angiogenesis • losartan • receptors, angiotensin II, PD 123319
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Angiotensin II has been shown to cause cell hypertrophy and hyperplasia in many tissues and cell types.1 2 3 4 5 The AT1 receptor has been implicated in the mediation of cardiac myocyte hypertrophy6 7 and vascular smooth muscle cell hyperplasia in large vessels.8 Less is known about the receptor mechanisms of the trophic actions of Ang II in the microvasculature.
In a study by Wang and Prewitt,9 microvascular density was reduced in hypertensive and normotensive rats treated with captopril for 4 weeks. Furthermore, Hernandez and colleagues10 showed that rats fed a high salt diet (4% NaCl) for 4 weeks also exhibited a reduction in microvascular density, which they attributed to suppression of the renin-angiotensin system caused by elevated salt intake. Chronic infusion of Ang II to maintain constant circulating Ang II levels blocked this reduction in microvessel density. Ang II has also been shown to stimulate angiogenesis in the corneal circulation and the developing chick chorioallantoic membrane model.3 4 11
Although Ang II has been shown to have trophic and angiogenic actions in the microcirculation, receptor mechanisms mediating these effects are not clear. This study confirms the vasoconstrictor and trophic activity of the AT1 receptor, which has previously been documented in larger vessels and other tissues, and indicates vasodilator and growth-inhibitory activity of the AT2 receptor.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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All procedures involving instrumentation and handling of animals were done in accordance with the National Institutes of Health Guidelines for the Care and Use of Laboratory Animals and were approved by the animal care committee at the Medical College of Wisconsin.
Surgical Implantation of Catheters
Seven- to 8-week-old (200
to 275 g) Sprague-Dawley
rats were placed on a high salt diet (4% NaCl, Dyets) 1 day before
surgery. Rats were anesthetized with ketamine (82 mg/kg
IM) and acepromazine (1.8 mg/kg IM). Polyvinyl chloride catheters were
placed in the left femoral artery and vein. Catheters were tunneled
subcutaneously and exited through the back between the scapulae. Groin
incisions were closed in layers with polyester suture. Catheters were
housed in a flexible spring that attached to a swivel device at the top
of the rat's cage. Dacron felt was affixed to a plate at the end of
the spring, which was placed subcutaneously. The incision was closed
over the plate with a polyester purse-string suture. Rats were
allowed to recover for 3 to 4 days.
BP Measurement
BP was measured for at least 1.5 hours at the
same time of day
on 2 control and 3 infusion days. Arterial BP and heart
rate were measured with Statham P23id pressure transducers connected to
a four-channel BP display unit (Stemtech). The analog signal was
low pass–filtered at 100 Hz, sampled at 300 Hz (model RTS-132,
Significat), and processed with software of our own design. Acquired
data were averaged in 1-minute intervals throughout the measurement
period.
Bolus Ang II Infusion
An Ang II bolus (25 ng/kg) was infused
through the venous line
on the first control day and last treatment day. BP responses were
recorded and analyzed for determination of the peak
change.
Chronic Agonist and Antagonist Infusions
Saline vehicle (0.9%
NaCl), Ang II (5 and 10 ng/kg per minute),
Ang II (5 ng/kg per minute) plus the selective AT1 receptor
antagonist losartan (a gift from DuPont, 2 and 20
µg/kg per minute) or the selective AT2 receptor
antagonist PD 123319 (a gift from Parke Davis, 0.5 and 5
µg/kg per minute), or antagonists alone were infused
through the venous catheters for 3 days with a syringe infusion pump
(Harvard Apparatus) at a rate of 1 mL/h. Solutions were
exchanged daily to prevent degradation of compounds.
Plasma Ang II Measurement
Plasma samples were drawn on the
first control day and last
treatment day into chilled tubes containing 0.125 mol/L
Na2EDTA and 0.025 mol/L phenanthroline. Samples were
centrifuged within 15 minutes of collection, and plasma was
separated and frozen at -70°C until extraction. Ang II
concentration in plasma was measured by the method of Nussberger et
al.12 Briefly, angiotensins were extracted
from plasma with a C18 column (Waters Associates) and eluted with
methanol. Ang II was separated from other angiotensin
metabolites by high-performance liquid
chromatography (HPLC) and measured by radioimmunoassay
with an antibody (kindly provided by Dr Charles Wood, University of
Florida) and [125I]iodotyrosyl4-Ang II (No.
IM177, Amersham). Recovery from C18 columns was 97% to 99%. Recovery
of radiolabeled Ang II from the HPLC column was 78%, and recovery of
unlabeled Ang II was 75%. Within-assay variability was less than
8% and between-assay variability was 26% to 30% on three pools
followed over 12 assays in 4 months. Variability of the concentration
at 50% of maximum binding was 6.29%.
Microvascular Density Measurement
At the end of the third
day, rats were killed by pentobarbital
overdose. Cremaster muscles were immediately harvested and cut into
quarters for analysis of vessel density. These sections were
fixed in 2% formalin for 3 days. The sections were immersed in 30
mg/mL rhodamine-labeled Griffonia simplicifolia I lectin
for 2 hours, rinsed several times in physiological
salt solution, and whole-mounted on a microscope slide with a
water-soluble mountant. Samples were then visualized at x200 with
a computerized video fluorescent microscope system with
epi-illumination (Olympus). Five to seven fields from each section
were randomly selected and saved for subsequent vessel density
measurement. We have previously shown that this technique
preferentially identifies small arterioles and
capillaries13 by binding to the basement membranes of
third- and fourth-order arterioles and capillaries. This renders
the technique insensitive to alterations in perfusion status and merely
identifies vessels that are intact.
Vessel density was determined by our previously described technique.9 Briefly, each microvascular image was enhanced by a series of digital image processing techniques with a commercial software package (Image-1, Universal Imaging Corp) and program of our own design.14 From this, a resultant line image of the network was created, and the intersections of the network and a computer-generated square grid overlay were automatically identified. Intersections within a 0.224-mm2 area field were automatically counted and provided a quantitative estimate of vessel density. Approximately 20 fields were counted and averaged from each rat.
Statistical Analysis
All results are presented as
mean±SE. Comparisons
between groups were made with a two-factor ANOVA with one repeat
(time). A value of P<.05 was considered significant.
Significant differences in BP between groups were further
analyzed with Bonferroni's method for multiple comparisons.
Significant differences in vessel density between groups were further
analyzed with Dunnett's method for comparison with a control
group (vehicle or Ang II, 5 ng/kg per minute). BP responses to bolus
Ang II were analyzed with a paired t test, as were
differences in plasma Ang II concentrations.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Plasma Ang II concentration in all groups (n=38) was 11.3±1.4 pg/mL before the start of infusion. After a 3-day infusion of Ang II with or without antagonists, plasma Ang II levels in paired samples increased significantly to 19.7±3.5 pg/mL. Paired Ang II levels did not change after a 3-day infusion of vehicle, PD 123319 alone, or Ang II plus PD 123319. In rats infused with Ang II alone (5 ng/kg per minute), plasma Ang II levels increased slightly (+3.4±2.2 pg/mL) but did not reach significance. Ang II levels increased significantly after treatment with Ang II plus losartan (18.5±4.3 pg/mL, n=15), Ang II plus losartan plus PD 123319 (26.3±7.1 pg/mL, n=4), and losartan alone (25.4±3.9 pg/mL, n=4).
Neither vehicle infusion nor Ang II infusion at 5 ng/kg per minute
resulted in a change in MAP over the infusion period. However, Ang II
infusion at a higher dose (10 ng/kg per minute) resulted in a large
increase in MAP (Fig 1
, top). Because we were interested
in the direct effects of Ang II on microvascular structure without the
confounding effects of elevated BP, Ang II was infused at 5 ng/kg per
minute in all groups coinfused with receptor antagonists.
In some of these groups, coinfusion did result in alterations in
BP.
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When the selective AT2 receptor antagonist PD
123319 was coinfused with the subpressor dose of Ang II (5 ng/kg per
minute), a low dose of the antagonist (0.5 µg/kg per
minute) did not alter MAP (Fig 1
, middle). When a higher dose
of
antagonist was coinfused (5 µg/kg per minute), a large
increase in MAP resulted which was similar to that seen with the
pressor dose of Ang II. Increasing concentrations of the selective
AT1 receptor antagonist losartan
coinfused with Ang II produced graded decreases in MAP (Fig 1,
bottom).
Heart rate did not change over time and was not different in any of the
infusion groups. Fig 2 shows the effects of infusion of
losartan alone (2 µg/kg per minute, n=4), PD 123319 alone (5
µg/kg per minute, n=6), and both antagonists infused with
Ang II (n=4). None of these groups showed a change in BP over time
compared with vehicle infusion alone.
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BP response to a 25 ng/kg bolus infusion of Ang II was determined
before the start of and after the chronic infusion treatment period to
confirm blockade of the receptors by the antagonists
(Table). Vehicle infusion had no effect, whereas the Ang
II–infused rats had an exaggerated bolus response after chronic
infusion. The group infused with the highest dose of PD 123319 (5
µg/kg per minute) showed no difference in bolus response after
chronic infusion. The group infused with the lower dose of PD 123319
(0.5 µg/kg per minute) showed a reduced bolus response after
infusion. However, in this group, preinfusion responses were abnormally
high compared with all other groups, and postinfusion responses in that
group were not different from those in the vehicle-infused group.
The groups receiving 2 and 20 µg/kg per minute losartan
exhibited a significantly blunted bolus response, suggesting adequate
blockade of the AT1 receptor.
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Measurement of microvascular density in the cremaster muscle showed an
increase in the number of capillaries and small arterioles in rats
infused with the subpressor dose of Ang II (5 ng/kg per minute)
compared with rats infused with vehicle (Fig 3, top).
Infusion of Ang II at the higher, pressor dose (10 ng/kg per minute)
resulted in no alteration in microvascular density. This agrees with
previous studies in which we have shown an effect of BP that opposes
angiogenesis.13 Coinfusion of PD 123319 with Ang II
produced a larger angiogenic response than with Ang II alone (Fig
3,
middle). Coinfusion of losartan with Ang II inhibited the
angiogenesis induced by Ang II at the lowest concentration of
losartan (Fig 3, bottom). Coinfusion of both
antagonists with Ang II resulted in a similar inhibition of
the angiogenic action of Ang II to AT1 antagonism (153±1.9
intersections, n=4). Infusion of either losartan or PD 123319
without coinfusion of Ang II resulted in no alteration in vessel
density compared with vehicle-infused controls (losartan,
-0.63±0.04%, n=4; PD 123319, -1.26±0.11%,
n=4).
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Fig 4 shows a comparison of the structural alterations
in the microvasculature among groups. Systemic infusion of Ang II at a
low concentration for 3 days resulted in marked angiogenesis (center)
compared with vehicle infusion (left). Selective blockade at the
AT2 receptor produced an even greater angiogenic response
(right).
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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This study suggests a role for the AT2 receptor in opposing the actions of the AT1 receptor. Evidence suggests that the AT1 receptor mediates vasoconstriction15 and vascular growth in the aorta and large arteries.8 Our results agree with these findings and show for the first time that Ang II induces angiogenesis in the microcirculation through the AT1 receptor. Our results also indicate that the AT2 receptor mediates vasodilation and inhibition of growth and tends to buffer the action of the more dominant AT1 receptor. The actions of the AT1 receptor may dominate in vivo because it may be the most prevalent angiotensin receptor in the vasculature. It has been shown to be expressed at a higher level than the AT2 receptor in the adult rat aorta16 ; however, the Ang II receptor populations in the microvasculature have not yet been characterized.
The current study showed that angiogenesis occurs after as few as 3 days of Ang II infusion and is the result of opposing forces of the AT1 and AT2 receptors. Previous studies have also shown a role for Ang II in microvascular proliferation.3 4 9 10 However, these studies were done using longer treatment periods and did not determine the receptor subtypes responsible for mediating this growth. LeNoble et al11 showed that CGP 42112, a then-putative AT2 antagonist, blocked Ang II–induced angiogenesis in the developing chick chorioallantoic membrane in a 7-day study. This compound is now considered to be a full AT2 agonist in many systems.17 If CGP 42112 was acting as an AT2 agonist in that study, then the results of LeNoble et al agree with ours, which suggest that the AT2 receptor has antiangiogenic activity. Unlike our findings, however, LeNoble et al did not observe any effect of losartan or PD 123319 on microvascular density. In receptor binding studies, the chick chorioallantoic membrane was shown to have a single class of receptor.11 CGP 42112 had moderate binding affinity for this class of receptor, whereas losartan and PD 123319 had extremely low affinity. This suggests that the avian receptor is markedly different from mammalian Ang II receptors, making determination of the relevance to mammalian systems difficult.
A result similar to our finding that stimulation of the AT2 receptor mediates a growth-inhibitory response in the microvasculature was shown in a recent study with cultured cells.18 That study showed that treatment of quiescent coronary artery endothelial cells with PD 123177 (an AT2 antagonist) and Ang II resulted in proliferation, whereas treatment with Ang II alone had no effect. This is further evidence that the stimulation of AT2 receptor acts as a brake to suppress cell growth during Ang II stimulation.
Another interesting result of the current study was the effect of the AT2 receptor on BP. Our results show that chronic infusion of PD 123319 causes an enhanced BP response to chronic but not acute Ang II infusion, suggesting that the AT2 receptor mediates vasodilation. This lack of an acute response of AT2 blockade as measured by bolus Ang II injections may explain the difference in results between this study and others aimed at illuminating the functions of the AT2 receptor. In a separate study, aortic rings stimulated with Ang II and PD 123319 produced a greater constriction than rings stimulated with Ang II alone.19 Another study showed a similar result with regard to the biphasic pressor response observed with bolus Ang III infusions.20 In that study, pretreatment of rats with PD 123319 resulted in an enhanced pressor response to Ang III, whereas pretreatment with losartan abolished the pressor response and exhibited an enhanced depressor response. Additional indirect evidence supporting our finding is that rat cerebral arteries, which express only the AT2 receptor subtype,21 vasodilate in response to Ang II stimulation.22 Although these findings do not rule out any role of central or renal effects of AT2 receptor inhibition on the alterations in BP we observed, they strongly suggest that Ang II causes vasodilation through stimulation of the AT2 receptor. In the present study, the effect of chronic Ang II and losartan coinfusion on BP was a losartan dose–dependent depressor response. The AT1 receptor is known to mediate vasoconstriction and so this response may be partly due to blockade of the AT1 receptor directly. However, since the Ang II dose being infused was already subpressor, this suggests that selective blockade of the AT1 receptor unmasked the vasodilator activity of the AT2 receptor, which resulted in an MAP below control (no Ang II infusion).
Losartan treatment resulted in a decrease in microvascular density compared with Ang II infusion alone; however, vessel density was still increased compared with control. In fact, we might have expected a decrease in vessel density to values lower than control because of blockade of the AT1-mediated angiogenic activity and unmasking of the AT2-mediated antiangiogenic activity. The reason for this result is not clear. Our bolus Ang II infusion data after 3 days of losartan infusion suggest complete blockade of the AT1 receptor. One confounding factor is the depressor response we saw in these groups. In the Ang II (10 ng/kg per minute) infusion group, an increased MAP appeared to inhibit the Ang II effect on vessel density. In previous studies, we have shown that in a renal hypertension model, the rise in pressure contributed to the reduction in vessel density.13 In a similar manner, a decrease in MAP such as was caused by losartan infusion may enhance the angiogenic effect. In fact, Hogan and Hirschmann23 found that a reduction in perfusion pressure of 30% in the rat cremaster muscle with normal flow induced arteriolar proliferation. It also is possible that losartan was spilling over and binding to the AT2 receptor as well as the AT1 receptor. This is unlikely because the bolus BP responses show a dose-dependent depressor response, indicating that the levels we are infusing are in the correct operating range for the AT1 receptor. Furthermore, the chronic BP data for the losartan- and PD 123319–infused groups exhibit differential effects by these antagonists, suggesting that the concentrations used are sufficient for selective receptor blockade. Experiments using both AT1 and AT2 receptor antagonists suggest no role for other receptor subtypes involved in the action of Ang II on vessel density or BP regulation in this model.
The effects of Ang II on BP and vessel density observed in this study required a very low Ang II concentration. In fact, Ang II levels in the plasma after infusion of Ang II alone were not significantly different from preinfusion levels. The increase in circulating Ang II was too small to be detected by our assay involving HPLC separation followed by radioimmunoassay yet was sufficient for detection by bioassay. The measured change of 3.4 pg/mL in the Ang II–infused group falls into the range of assay variability and so may be less sensitive than our bioassay. This phenomenon has been documented in other hormone systems as well.24 25 Because high salt intake results in suppression of the intrinsic renin-angiotensin system, Ang II receptor populations may have been upregulated and the system may be more responsive to low levels of Ang II. Also, the most dramatic responses to Ang II stimulation in both BP and vessel density occurred during selective receptor blockade. Because the respective actions of the two receptor types balance each other out to a great extent, blockade of one receptor was necessary to reveal the activity of the opposing receptor. Thus, a subpressor concentration of Ang II becomes pressor with AT2 receptor blockade and depressor with AT1 blockade.
The results from this short-term Ang II infusion study differ from those from an earlier study from this laboratory.10 Although we detected no alteration in MAP after Ang II infusion at 5 ng/kg per minute in the present study, we found Ang II infusion at a rate of 10 ng/kg per minute to be pressor. In contrast, Hernandez et al10 showed Ang II doses of both 5 and 10 ng/kg per minute to be subpressor. That study assessed BP and vessel density changes after 4 weeks of Ang II infusion compared with 3 days in the present study. It is likely that long-term BP regulation compensated for any elevation of BP caused by Ang II infusion in the 4-week study that was not apparent in our 3-day study. This inherent difference between the two studies helps to explain the difference in the angiogenic activity of Ang II observed. In both studies, the 5 ng/kg per minute dose was found to be angiogenic. In the 4-week study, the 10 ng/kg per minute dose was found to be angiogenic, whereas it was ineffective in stimulating vessel growth in the 3-day study. This may be due to the fact that the dose was pressor in the 3-day study, which may have counteracted the angiogenesis. This observation that elevated BP inhibits the angiogenic action of Ang II is consistent throughout the present study, with one exception. Ang II coinfused with PD 123319 (5 µg/kg per minute) caused an increase in both MAP and vessel density. Apparently, in the presence of AT2 receptor blockade, the angiogenic stimulus is so strong it overrides the inhibitory influence of elevated MAP. It is possible that if MAP were artificially held constant in the face of maximal AT2 receptor antagonism, the resulting angiogenesis would be even greater.
In the present study, short-term Ang II infusion resulted in an increase in microvascular density. This angiogenesis appeared to be mediated by the AT1 receptor, whereas the AT2 receptor mediated antiangiogenesis, buffering the full AT1 growth response when both receptors were activated. In addition, the AT1 receptor mediated an increase in MAP in this study, and the AT2 receptor mediated a depressor response that similarly acted to buffer the full AT1 pressor response when both receptors were activated. These results fit well with previous findings in large vessels and other cell and tissue types and offer new insight into the mechanisms that may be involved in microvascular remodeling. Potential differential regulation of these receptor subtypes in disease states such as diabetes or hypertension may prove to be a factor in the development of microvascular pathology.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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The authors would like to thank Jennifer Clark for expert technical assistance.
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References |
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TopAbstractIntroductionMethods Results Discussion References |
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 Kai Chen, D. C. Merrill, and J. C. Rose The Importance of Angiotensin II Subtype Receptors for Blood Pressure Control During Mouse Pregnancy Reproductive Sciences, October 1, 2007; 14(7): 694 - 704. [Abstract] [PDF]
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K. Rakusan, Z. Chvojkova, P. Oliviero, I. Ostadalova, F. Kolar, C. Chassagne, J.-L. Samuel, and B. Ostadal ANG II type 1 receptor antagonist irbesartan inhibits coronary angiogenesis stimulated by chronic intermittent hypoxia in neonatal rats Am J Physiol Heart Circ Physiol, March 1, 2007; 292(3): H1237 - H1244. [Abstract] [Full Text] [PDF]
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 P. K. Mehta and K. K. Griendling Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system Am J Physiol Cell Physiol, January 1, 2007; 292(1): C82 - C97. [Abstract] [Full Text] [PDF]
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F. Feihl, L. Liaudet, B. Waeber, and B. I. Levy Hypertension: A Disease of the Microcirculation? Hypertension, December 1, 2006; 48(6): 1012 - 1017. [Full Text] [PDF]
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 M. Ushio-Fukai Redox signaling in angiogenesis: Role of NADPH oxidase Cardiovasc Res, July 15, 2006; 71(2): 226 - 235. [Abstract] [Full Text] [PDF]
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M. C. Petersen, D. H. Munzenmaier, and A. S. Greene Angiotensin II infusion restores stimulated angiogenesis in the skeletal muscle of rats on a high-salt diet Am J Physiol Heart Circ Physiol, July 1, 2006; 291(1): H114 - H120. [Abstract] [Full Text] [PDF]
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M. M. de Resende, S. L. Amaral, D. H. Munzenmaier, and A. S. Greene Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake Physiol Genomics, April 13, 2006; 25(2): 325 - 335. [Abstract] [Full Text] [PDF]
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D. H. Munzenmaier and A. S. Greene Chronic angiotensin II AT1 receptor blockade increases cerebral cortical microvessel density Am J Physiol Heart Circ Physiol, February 1, 2006; 290(2): H512 - H516. [Abstract] [Full Text] [PDF]
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A. D'Amore, M. J. Black, and W. G. Thomas The Angiotensin II Type 2 Receptor Causes Constitutive Growth of Cardiomyocytes and Does Not Antagonize Angiotensin II Type 1 Receptor-Mediated Hypertrophy Hypertension, December 1, 2005; 46(6): 1347 - 1354. [Abstract] [Full Text] [PDF]
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 J. Zheng, I. M. Bird, D.-B. Chen, and R. R. Magness Angiotensin II regulation of ovine fetoplacental artery endothelial functions: interactions with nitric oxide J. Physiol., May 15, 2005; 565(1): 59 - 69. [Abstract] [Full Text] [PDF]
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L. M. Duke, R. G. Evans, and R. E Widdop AT2 receptors contribute to acute blood pressure-lowering and vasodilator effects of AT1 receptor antagonism in conscious normotensive but not hypertensive rats Am J Physiol Heart Circ Physiol, May 1, 2005; 288(5): H2289 - H2297. [Abstract] [Full Text] [PDF]
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J. P. Forder, D. H. Munzenmaier, and A. S. Greene Angiogenic protection from focal ischemia with angiotensin II type 1 receptor blockade in the rat Am J Physiol Heart Circ Physiol, April 1, 2005; 288(4): H1989 - H1996. [Abstract] [Full Text] [PDF]
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 E. Vazquez, I. Coronel, R. Bautista, E. Romo, C. M. Villalon, M. C. Avila-Casado, V. Soto, and B. Escalante Angiotensin II-dependent induction of AT2 receptor expression after renal ablation Am J Physiol Renal Physiol, January 1, 2005; 288(1): F207 - F213. [Abstract] [Full Text] [PDF]
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 B. I. Levy Can Angiotensin II Type 2 Receptors Have Deleterious Effects in Cardiovascular Disease?: Implications for Therapeutic Blockade of the Renin-Angiotensin System Circulation, January 6, 2004; 109(1): 8 - 13. [Full Text] [PDF]
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 H. Thai, J. Wollmuth, S. Goldman, and M. Gaballa Angiotensin Subtype 1 Receptor (AT1) Blockade Improves Vasorelaxation in Heart Failure by Up-Regulation of Endothelial Nitric-Oxide Synthase via Activation of the AT2 Receptor J. Pharmacol. Exp. Ther., December 1, 2003; 307(3): 1171 - 1178. [Abstract] [Full Text] [PDF]
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 H. Uemura, H. Ishiguro, N. Nakaigawa, Y. Nagashima, Y. Miyoshi, K. Fujinami, A. Sakaguchi, and Y. Kubota Angiotensin II receptor blocker shows antiproliferative activity in prostate cancer cells: A possibility of tyrosine kinase inhibitor of growth factor Mol. Cancer Ther., November 1, 2003; 2(11): 1139 - 1147. [Abstract] [Full Text] [PDF]
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R. Benndorf, R. H. Boger, S. Ergun, A. Steenpass, and T. Wieland Angiotensin II Type 2 Receptor Inhibits Vascular Endothelial Growth Factor-Induced Migration and In Vitro Tube Formation of Human Endothelial Cells Circ. Res., September 5, 2003; 93(5): 438 - 447. [Abstract] [Full Text] [PDF]
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 S. Sarlos, B. Rizkalla, C. J. Moravski, Z. Cao, M. E. Cooper, and J. L. Wilkinson-Berka Retinal Angiogenesis Is Mediated by an Interaction between the Angiotensin Type 2 Receptor, VEGF, and Angiopoietin Am. J. Pathol., September 1, 2003; 163(3): 879 - 887. [Abstract] [Full Text] [PDF]
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B. Yuan, M. Liang, Z. Yang, E. Rute, N. Taylor, M. Olivier, and A. W. Cowley Jr. Gene expression reveals vulnerability to oxidative stress and interstitial fibrosis of renal outer medulla to nonhypertensive elevations of ANG II Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2003; 284(5): R1219 - R1230. [Abstract] [Full Text] [PDF]
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T. Shimizu, H. Okamoto, S. Chiba, Y. Matsui, T. Sugawara, M. Akino, J. Nan, H. Kumamoto, H. Onozuka, T. Mikami, et al. VEGF-mediated angiogenesis is impaired by angiotensin type 1 receptor blockade in cardiomyopathic hamster hearts Cardiovasc Res, April 1, 2003; 58(1): 203 - 212. [Abstract] [Full Text] [PDF]
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R. A. de Boer, Y. M. Pinto, A. J.H. Suurmeijer, S. Pokharel, E. Scholtens, M. Humler, J. M. Saavedra, F. Boomsma, W. H. van Gilst, and D. J. van Veldhuisen Increased expression of cardiac angiotensin II type 1 (AT1) receptors decreases myocardial microvessel density after experimental myocardial infarction Cardiovasc Res, February 1, 2003; 57(2): 434 - 442. [Abstract] [Full Text] [PDF]
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L. Loufrani, B. I. Levy, and D. Henrion Defect in Microvascular Adaptation to Chronic Changes in Blood Flow in Mice Lacking the Gene Encoding for Dystrophin Circ. Res., December 13, 2002; 91(12): 1183 - 1189. [Abstract] [Full Text] [PDF]
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 U. Rueckschloss, M. T. Quinn, J. Holtz, and H. Morawietz Dose-Dependent Regulation of NAD(P)H Oxidase Expression by Angiotensin II in Human Endothelial Cells: Protective Effect of Angiotensin II Type 1 Receptor Blockade in Patients With Coronary Artery Disease Arterioscler Thromb Vasc Biol, November 1, 2002; 22(11): 1845 - 1851. [Abstract] [Full Text] [PDF]
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S. Jesmin, Y. Hattori, I. Sakuma, C. N. Mowa, and A. Kitabatake Role of ANG II in coronary capillary angiogenesis at the insulin-resistant stage of a NIDDM rat model Am J Physiol Heart Circ Physiol, October 1, 2002; 283 (4): H1387 - H1397. [Abstract] [Full Text] [PDF]
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J.-S. Silvestre, R. Tamarat, T. Senbonmatsu, T. Icchiki, T. Ebrahimian, M. Iglarz, S. Besnard, M. Duriez, T. Inagami, and B. I. Levy Antiangiogenic Effect of Angiotensin II Type 2 Receptor in Ischemia-Induced Angiogenesis in Mice Hindlimb Circ. Res., May 31, 2002; 90(10): 1072 - 1079. [Abstract] [Full Text] [PDF]
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M. P. Schuijt, P. R. Saxena, A.H. J. Danser, R. M. Carey, N. L. Howell, X.-H. Jin, and H. M. Siragy No Net Effect of Angiotensin II on Blood Pressure? * Response Hypertension, May 1, 2002; 39 (5): e27 - e28. [Full Text] [PDF]
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R. Tamarat, J.-S. Silvestre, N. Kubis, J. Benessiano, M. Duriez, M. deGasparo, D. Henrion, and B. I. Levy Endothelial Nitric Oxide Synthase Lies Downstream From Angiotensin II-Induced Angiogenesis in Ischemic Hindlimb Hypertension, March 1, 2002; 39(3): 830 - 835. [Abstract] [Full Text] [PDF]
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M. Stoll, A. W.A. Hahn, U. Jonas, Y. Zhao, B. Schieffer, J. W. Fischer, and T. Unger Identification of a Zinc Finger Homoeodomain Enhancer Protein After AT2 Receptor Stimulation by Differential mRNA Display Arterioscler Thromb Vasc Biol, February 1, 2002; 22(2): 231 - 237. [Abstract] [Full Text] [PDF]
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C. Berry, R. Touyz, A. F. Dominiczak, R. C. Webb, and D. G. Johns Angiotensin receptors: signaling, vascular pathophysiology, and interactions with ceramide Am J Physiol Heart Circ Physiol, December 1, 2001; 281(6): H2337 - H2365. [Abstract] [Full Text] [PDF]
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M. P. Schuijt, M. Basdew, R. van Veghel, R. de Vries, P. R. Saxena, R. G. Schoemaker, and A. H. Jan Danser AT2 receptor-mediated vasodilation in the heart: effect of myocardial infarction Am J Physiol Heart Circ Physiol, December 1, 2001; 281(6): H2590 - H2596. [Abstract] [Full Text] [PDF]
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 K.H. Schauser, A.H. Nielsen, H. Winther, V. Dantzer, and K. Poulsen Localization of the Renin-Angiotensin System in the Bovine Ovary: Cyclic Variation of the Angiotensin II Receptor Expression Biol Reprod, December 1, 2001; 65(6): 1672 - 1680. [Abstract] [Full Text] [PDF]
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R. M. Carey, N. L. Howell, X.-H. Jin, and H. M. Siragy Angiotensin Type 2 Receptor-Mediated Hypotension in Angiotensin Type-1 Receptor-Blocked Rats Hypertension, December 1, 2001; 38(6): 1272 - 1277. [Abstract] [Full Text] [PDF]
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J. Deinum, J. M.G. van Gool, M. J.M. Kofflard, F. J. ten Cate, and A.H. J. Danser Angiotensin II Type 2 Receptors and Cardiac Hypertrophy in Women With Hypertrophic Cardiomyopathy Hypertension, December 1, 2001; 38(6): 1278 - 1281. [Abstract] [Full Text] [PDF]
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D. Henrion, N. Kubis, and B. I. Levy Physiological and Pathophysiological Functions of the AT2 Subtype Receptor of Angiotensin II: From Large Arteries to the Microcirculation Hypertension, November 1, 2001; 38(5): 1150 - 1157. [Abstract] [Full Text] [PDF]
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S. L. Amaral, P. E. Papanek, and A. S. Greene Angiotensin II and VEGF are involved in angiogenesis induced by short-term exercise training Am J Physiol Heart Circ Physiol, September 1, 2001; 281(3): H1163 - H1169. [Abstract] [Full Text] [PDF]
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J. W Fischer, M. Stoll, A. W.A Hahn, and T. Unger Differential regulation of thrombospondin-1 and fibronectin by angiotensin II receptor subtypes in cultured endothelial cells Cardiovasc Res, September 1, 2001; 51(4): 784 - 791. [Abstract] [Full Text] [PDF]
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D. S. Weber and J. H. Lombard Angiotensin II AT1 receptors preserve vasodilator reactivity in skeletal muscle resistance arteries Am J Physiol Heart Circ Physiol, May 1, 2001; 280(5): H2196 - H2202. [Abstract] [Full Text] [PDF]
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A. F. Moore, N. T. Heiderstadt, E. Huang, N. L. Howell, Z.-Q. Wang, H. M. Siragy, and R. M. Carey Selective Inhibition of the Renal Angiotensin Type 2 Receptor Increases Blood Pressure in Conscious Rats Hypertension, May 1, 2001; 37(5): 1285 - 1291. [Abstract] [Full Text] [PDF]
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J. M. Saavedra, W. Hauser, G. Ciuffo, G. Egidy, K.-L. Hoe, O. Johren, T. Sembonmatsu, T. Inagami, and I. Armando Increased AT1 receptor expression and mRNA in kidney glomeruli of AT2 receptor gene-disrupted mice Am J Physiol Renal Physiol, January 1, 2001; 280(1): F71 - F78. [Abstract] [Full Text] [PDF]
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 D. FLISER, R. DIKOW, S. DEMUKAJ, and E. RITZ Opposing Effects of Angiotensin II on Muscle and Renal Blood Flow under Euglycemic Conditions J. Am. Soc. Nephrol., November 1, 2000; 11(11): 2001 - 2006. [Abstract] [Full Text]
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 M. de Gasparo, K. J. Catt, T. Inagami, J. W. Wright, and Th. Unger International Union of Pharmacology. XXIII. The Angiotensin II Receptors Pharmacol. Rev., September 1, 2000; 52(3): 415 - 472. [Abstract] [Full Text] [PDF]
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T. R. Nurkiewicz and M. A. Boegehold Reinforcement of arteriolar myogenic activity by endogenous ANG II: susceptibility to dietary salt Am J Physiol Heart Circ Physiol, July 1, 2000; 279(1): H269 - H278. [Abstract] [Full Text] [PDF]
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S. Engeli, R. Negrel, and A. M. Sharma Physiology and Pathophysiology of the Adipose Tissue Renin-Angiotensin System Hypertension, June 1, 2000; 35(6): 1270 - 1277. [Abstract] [Full Text] [PDF]
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 S. Gallinat, S. Busche, M. K. Raizada, and C. Sumners The angiotensin II type 2 receptor: an enigma with multiple variations Am J Physiol Endocrinol Metab, March 1, 2000; 278(3): E357 - E374. [Abstract] [Full Text] [PDF]
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S. B. Parker, A. D. Dobrian, S. S. Wade, and R. L. Prewitt AT1 receptor inhibition does not reduce arterial wall hypertrophy or PDGF-A expression in renal hypertension Am J Physiol Heart Circ Physiol, February 1, 2000; 278(2): H613 - H622. [Abstract] [Full Text] [PDF]
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R. M. Carey, Z.-Q. Wang, and H. M. Siragy Role of the Angiotensin Type 2 Receptor in the Regulation of Blood Pressure and Renal Function Hypertension, January 1, 2000; 35(1): 155 - 163. [Abstract] [Full Text] [PDF]
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 E. Chamoux Involvement of the Angiotensin II Type 2 Receptor in Apoptosis during Human Fetal Adrenal Gland Development J. Clin. Endocrinol. Metab., December 1, 1999; 84(12): 4722 - 4730. [Abstract] [Full Text]
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X. RUAN, M. I. OLIVERIO, T. M. COFFMAN, and W. J. ARENDSHORST Renal Vascular Reactivity in Mice: AngII-Induced Vasoconstriction inAT1A Receptor Null Mice J. Am. Soc. Nephrol., December 1, 1999; 10(12): 2620 - 2630. [Abstract] [Full Text]
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T. J. Bivalacqua, A. Dalal, H. C. Champion, and P. J. Kadowitz Role of AT1 receptors and autonomic nervous system in mediating acute pressor responses to ANG II in anesthetized mice Am J Physiol Endocrinol Metab, November 1, 1999; 277(5): E838 - E847. [Abstract] [Full Text] [PDF]
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M. N. Barber, D. B. Sampey, and R. E. Widdop AT2 Receptor Stimulation Enhances Antihypertensive Effect of AT1 Receptor Antagonist in Hypertensive Rats Hypertension, November 1, 1999; 34(5): 1112 - 1116. [Abstract] [Full Text] [PDF]
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 F. Cote, T. H. Do, L. Laflamme, J.-M. Gallo, and N. Gallo-Payet Activation of the AT2 Receptor of Angiotensin II Induces Neurite Outgrowth and Cell Migration in Microexplant Cultures of the Cerebellum J. Biol. Chem., October 29, 1999; 274(44): 31686 - 31692. [Abstract] [Full Text] [PDF]
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 L. Gendron*, L. Laflamme*, N. Rivard, C. Asselin, M. D. Payet, and N. Gallo-Payet Signals from the AT2 (Angiotensin Type 2) Receptor of Angiotensin II Inhibit p21ras and Activate MAPK (Mitogen-Activated Protein Kinase) to Induce Morphological Neuronal Differentiation in NG108-15 Cells Mol. Endocrinol., September 1, 1999; 13(9): 1615 - 1626. [Abstract] [Full Text]
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J.-E. Fabre, A. Rivard, M. Magner, M. Silver, and J. M. Isner Tissue Inhibition of Angiotensin-Converting Enzyme Activity Stimulates Angiogenesis In Vivo Circulation, June 15, 1999; 99(23): 3043 - 3049. [Abstract] [Full Text] [PDF]
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I. Tritto and G. Ambrosio Spotlight on microcirculation: an update Cardiovasc Res, June 1, 1999; 42(3): 600 - 606. [Full Text] [PDF]
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M. Horiuchi, M. Akishita, and V. J. Dzau Recent Progress in Angiotensin II Type 2 Receptor Research in the Cardiovascular System Hypertension, February 1, 1999; 33(2): 613 - 621. [Abstract] [Full Text] [PDF]
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M. Tamura, Y. Wanaka, E. J. Landon, and T. Inagami Intracellular Sodium Modulates the Expression of Angiotensin II Subtype 2 Receptor in PC12W Cells Hypertension, February 1, 1999; 33(2): 626 - 632. [Abstract] [Full Text] [PDF]
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E. H. Nora, D. H. Munzenmaier, F. M. Hansen-Smith, J. H. Lombard, and A. S. Greene Localization of the ANG II type 2 receptor in the microcirculation of skeletal muscle Am J Physiol Heart Circ Physiol, October 1, 1998; 275(4): H1395 - H1403. [Abstract] [Full Text] [PDF]
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H.J.M. G. Nelissen-Vrancken, M. C. Kuizinga, M. J.A.P. Daemen, and J. F.M. Smits Early captopril treatment inhibits DNA synthesis in endothelial cells and normalization of maximal coronary flow in infarcted rat hearts Cardiovasc Res, October 1, 1998; 40(1): 156 - 164. [Abstract] [Full Text] [PDF]
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 R. Lucius, S. Gallinat, P. Rosenstiel, T. Herdegen, J. Sievers, and T. Unger The Angiotensin II Type 2 (AT2) Receptor Promotes Axonal Regeneration in the Optic Nerve of Adult Rats J. Exp. Med., August 17, 1998; 188(4): 661 - 670. [Abstract] [Full Text] [PDF]
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M. M. Muthalif, I. F. Benter, M. R. Uddin, J. L. Harper, and K. U. Malik Signal Transduction Mechanisms Involved in Angiotensin-(1-7)-Stimulated Arachidonic Acid Release and Prostanoid Synthesis in Rabbit Aortic Smooth Muscle Cells J. Pharmacol. Exp. Ther., January 1, 1998; 284(1): 388 - 398. [Abstract] [Full Text]
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D. Fliser, F. Schaefer, D. Schmid, J. D. Veldhuis, and E. Ritz Angiotensin II Affects Basal, Pulsatile, and Glucose-Stimulated Insulin Secretion in Humans Hypertension, November 1, 1997; 30(5): 1156 - 1161. [Abstract] [Full Text]
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M. J. Rieder, R. Carmona, J. E. Krieger, K. A. Pritchard Jr, and A. S. Greene Suppression of Angiotensin-Converting Enzyme Expression and Activity by Shear Stress Circ. Res., March 1, 1997; 80(3): 312 - 319. [Abstract] [Full Text]
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L. Xu and V. L. Brooks Sodium Intake, Angiotensin II Receptor Blockade, and Baroreflex Function in Conscious Rats Hypertension, January 1, 1997; 29(1): 450 - 457. [Abstract] [Full Text] [PDF]
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P. Gohlke, I. Kuwer, A. Schnell, K. Amann, G. Mall, and T. Unger Blockade of Bradykinin B2 Receptors Prevents the Increase in Capillary Density Induced by Chronic Angiotensin-Converting Enzyme Inhibitor Treatment in Stroke-Prone Spontaneously Hypertensive Rats Hypertension, January 1, 1997; 29(1): 478 - 482. [Abstract] [Full Text] [PDF]
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 F. H. Messerli, M. A. Weber, and H. R. Brunner Angiotensin II Receptor Inhibition: A New Therapeutic Principle Arch Intern Med, September 23, 1996; 156(17): 1957 - 1965. [Abstract] [PDF]
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J.-S. Silvestre, S. Bergaya, R. Tamarat, M. Duriez, C. M. Boulanger, and B. I. Levy Proangiogenic Effect of Angiotensin-Converting Enzyme Inhibition Is Mediated by the Bradykinin B2 Receptor Pathway Circ. Res., October 12, 2001; 89(8): 678 - 683. [Abstract] [Full Text] [PDF]
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