doi: 10.1161/hy1101.095329
(Hypertension. 2001;38:1049.)
© 2001 American Heart Association, Inc.
Scientific Contributions |
Endothelium-Derived Nitric Oxide Regulates Arterial Elasticity in Human Arteries In Vivo
From the Cardiovascular Division, Brigham and Women’s Hospital, Boston, Mass.
Correspondence to Scott Kinlay, MBBS, PhD, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115. E-mail skinlay{at}rics.bwh.harvard.edu
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Abstract |
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Abstract—— Arterial elasticity is determined by structural characteristics of the artery wall and by vascular smooth muscle tone. The identity of endogenous vasoactive substances that regulate elasticity has not been defined in humans. We hypothesized that NO, a vasodilator released constitutively by the endothelium, augments arterial elasticity. Seven healthy young men were studied. A 20-MHz intravascular ultrasound catheter was introduced through an arterial sheath to measure brachial artery cross-sectional area, wall thickness, and intra-arterial pressure. After control was established, indices of elasticity (pressure-area relationship, instantaneous compliance, and stress-strain, pressure–incremental elastic modulus (Einc), and pressure–pulse wave velocity relationships) were examined over 0 to 100 mm Hg transmural pressure obtained by inflation of an external cuff. Thereafter, the basal production of endothelium-derived NO was inhibited by NG-monomethyl-L-arginine (L-NMMA) (4 and 8 mg/min). Finally, nitroglycerin (2.5 and 12.5 µg/min), an exogenous donor of NO, was given to relax the vascular smooth muscle. Elasticity was measured under all of these conditions. L-NMMA (8 mg/min) decreased brachial artery area (P=0.016) and compliance (P<0.0001) and increased Einc (P<0.01) and pulse wave velocity (P<0.0001). Nitroglycerin (12.5 µg/min) increased brachial artery area (P<0.001) and compliance (P<0.001) and decreased pulse wave velocity (P=0.02). NO, an endothelium-derived vasodilator, augments arterial elasticity in the human brachial artery. Loss of constitutively released NO associated with cardiovascular risk factors may adversely affect arterial elasticity in humans.
Key Words: brachial artery • elasticity • human • endothelium-derived relaxing factor
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Introduction |
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Elasticity of large arteries absorbs the energy of the phasic stroke volume in systole and thereby dampens the arterial pressure wave during its propagation through the arterial tree.1 The release of stored energy in diastole facilitates the continuous flow of blood to tissues.2
Several indices of arterial elasticity have been used in clinical studies, including compliance, distensibility index, stress-strain relationships, Young’s modulus, and pulse wave velocity. Arterial compliance refers to the relationship between arterial dimension and the distending pressure. An increase in compliance corresponds to a decrease in artery stiffness. Arterial compliance changes in a nonlinear fashion with blood pressure. It tends to be greater at lower blood pressures, and for this reason the distensibility index (change in volume/change in pressurexbaseline volume) can lead to erroneous conclusions if the mean distending pressure is shifted by an intervention. Compliance curves and the incremental modulus (Einc) can be used to assess elasticity independent of the blood pressure changes. Recently, a technique to assess arterial elasticity in humans with the use of intravascular ultrasound to measure arterial dimension and inflation of an external blood pressure cuff to generate a range of distending pressures has been described.3 This approach has been used to assess the effect of different structural components that contribute to arterial elasticity, including collagen, elastin, and vascular smooth muscle.4
In addition to the passive contribution of these constituents in the arterial wall, the active component of elasticity in vivo relates to the vascular smooth muscle tone. Prior studies have administered pharmacological vasoactive agents that directly affect smooth muscle tone to study this active component.3,5 However, in healthy arteries the continuous production of NO, an endothelium-derived vasodilator, regulates vascular tone and arterial dimension.6 Therefore, we investigated whether this endogenous substance plays a significant physiological role in controlling arterial elasticity.
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Methods |
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Seven healthy young men were recruited by newspaper advertisements. Written informed consent was obtained from all subjects, and the study was approved by the Brigham and Women’s Hospital Human Research Committee.
Experimental Protocol
All subjects were studied in a quiet room with a constant temperature (23°C). A 20-MHz 3.4F Visions Five-64 intravascular ultrasound catheter (Endosonics) was inserted into the brachial artery via a 4F arterial sheath. The side arm of the arterial sheath was connected to a Statham P23 pressure transducer (Gould Statham Instruments), and the arterial waveforms were recorded onto a physiological recorder (Gould) together with the ECG. The pharmacological agents were infused into the guidewire channel of the intravascular ultrasound catheter to enter the brachial artery approximately 10 mm upstream of the ultrasound crystals (Figure 1).
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A control solution of 5% dextrose was infused with a Harvard pump (Harvard Apparatus) at 1 mL/min for 8 minutes, followed by the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) at 4 (16 µmol/min) and 8 mg/min (32 µmol/min) for 4 minutes each, then nitroglycerin, a NO donor, at 2.5 and 12.5 µg/min for 4 minutes each.
A 12-cm blood pressure cuff was placed around the upper arm and centered over the ultrasound crystals on the intravascular ultrasound catheter. This cuff was inflated by 10-mm Hg increments to generate a range of transmural distending pressures (intra-arterial minus cuff pressure) below the diastolic pressure during each of the 5 infusions.3
Image Analysis
The intravascular ultrasound images were digitized from the videotape. The lumen cross-sectional area and wall thickness were measured by computerized planimetry (TapeMeasure, INDEC Systems) by 1 operator blinded to the drug infusions and stage in the cardiac cycle. Diastolic images from the cardiac cycle were measured to avoid any errors due to the inertial and viscous behaviors of the arterial wall during systole.3 The images from 4 cardiac cycles were averaged for each pressure increment. The arterial thickness was measured adjacent to a vein.3
Calculations of Elastic Properties
The method for estimating arterial elasticity has been described previously.3,5 Briefly, the transmural pressure versus cross-sectional area data were plotted for each of the 5 infusions. Each curve was fitted to the formula of Langewouters et al,7 A=a[0.5+1/
tan-1(P/c-b/c)], where A is cross-sectional area, P is transmural pressure, and a, b, and c are 3 independent parameters that characterize each pressure-area curve, by using nonlinear least-squares regression methods. Brachial artery instantaneous compliance, circumferential wall stress, wall strain, Einc, and pulse wave velocity were calculated as described previously.3,5
Statistical Analysis
The curves generated by each infusion were compared by general linear mixed effects models in SAS. Area, compliance, and strain were log transformed to generate more linear relationships with the covariates. Interaction terms were used to assess nonparallel shifts in the curves. We performed post hoc pairwise comparisons of the infusions compared with control using the Dunnett-Hsu correction for multiple comparisons, with statistical significance set at P<0.05.
An expanded Methods section can be found in an online data supplement available at http://www.hypertensionaha.org.
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Results |
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Patient Population
We studied 7 healthy young men age 23 to 33 years (mean±SD age, 28±4 years). Mean±SD values were as follows: systolic blood pressure, 116±11 mm Hg; diastolic pressure, 67±5 mm Hg; total cholesterol, 169±33 mg/dL; LDL cholesterol, 98±34 mg/dL; and body mass index, 23.8±2.2 kg/m2.
Effects of NO on Brachial Artery Pressure-Area Relationship and Compliance
Figure 2 (top) shows the transmural pressure versus cross-sectional area relationships. There were significant nonparallel differences among the various experimental conditions on the pressure-area curves (P<0.02). Compared with control infusion, there was an increase in cross-sectional area with nitroglycerin (12.5 µg/min; P<0.001) and a reduction in area with L-NMMA (8 mg/min; P=0.016) across all transmural pressures.
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The transmural pressure versus compliance relationships are shown in Figure 2 (bottom). There was a significant nonparallel difference between the experimental conditions on the pressure curves (P<0.001). Compared with control, nitroglycerin increased compliance (12.5 µg/min; P<0.0001), and L-NMMA reduced compliance (8 mg/min; P<0.0001). In a separate analysis that confined the examination of the effects of the infusions to the physiological range of transmural pressures (60 to 100 mm Hg), compliance increased with nitroglycerin (12.5 µg/min; P<0.001) and decreased with L-NMMA (8 mg/min; P<0.05).
Effects on Stress, Strain, Einc, and Pulse Wave Velocity
Wall stress versus strain relationships are shown in Figure 3. Nitroglycerin significantly shifted the curves to the right (12.5 µg/min; P<0.001), and L-NMMA shifted the curve to the left (8 mg/min; P<0.02).
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Figure 4 shows the isometric and isobaric Einc relationships. At constant Einc, strain was significantly higher with nitroglycerin (12.5 µg/min; P<0.0001) and was significantly reduced with L-NMMA (8 mg/min; P<0.002). Under isobaric conditions, there was a significant increase in Einc with L-NMMA (8 mg/min; P<0.0001), while nitroglycerin returned Einc to baseline.
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Figure 5 shows the pulse wave velocity versus transmural pressure relationships. There was a significant increase in pulse wave velocity with L-NMMA (8 mg/min; P<0.0001) and a decrease in pulse wave velocity with nitroglycerin (12.5 µg/min; P=0.02).
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Discussion |
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The novel finding of this study is that the constitutive release of NO contributes to arterial elasticity in healthy humans. We used intravascular ultrasound to assess elasticity of the brachial artery by measuring its cross-sectional area and wall thickness over a range of luminal distending pressures, generated by inflation of an external blood pressure cuff. Inhibition of NO synthase with L-NMMA consistently affected all measures of arterial elasticity. It reduced arterial compliance, shifted the stress-strain and Einc-stress curves to the right, increased Einc under isometric and isobaric conditions, and increased pulse wave velocity.
Although the methodology we used is invasive, it yields rigorous measures of arterial elasticity in vivo by relating changes in artery caliber to changes in pressure over a wide range of transmural pressures. Furthermore, our analysis is derived from diastolic images that assess the pure elastic behavior of the artery and not the viscous or inertial behavior exhibited during the rapid stretch of systole.3 The consistent results among several measures of elasticity, each emphasizing a somewhat different aspect of arterial stiffness,3 and the dose-response effects strengthen our results and conclusions.
A previous study found that the basal release of NO paradoxically reduced arterial compliance.8 In that study compliance was measured by external ultrasound with wall tracking over a more restricted range of arterial pressure, and a lower concentration of L-NMMA (10-6 mol/min) was used. In contrast, we evaluated elasticity across a broad range of distending pressures generated by the use of an external cuff, and we used a higher concentration of L-NMMA previously shown to nearly completely inhibit NO bioavailability.9 By using area and pressure measurements from diastole, we also avoided the viscous and inertial components of arterial distention during the rapid changes in systole, thereby more accurately defining the changes in arterial elasticity with loss of NO.
Arterial elasticity has 2 major elements: a passive component that reflects the structural composition of the artery wall and an active component related to arterial tone.4 The latter reflects the anatomic "in series" linkage of vascular smooth muscle cells with connective tissue.10 Accordingly, pharmacological vasoconstrictors typically reduce and vasodilators augment arterial elasticity.3,5,11,12 The locally released vasoactive substances that might regulate arterial elasticity in healthy humans have not been well defined. Because NO, an endothelium-derived vasodilator, is released constitutively, we postulated that it improves the elastic behavior of arteries and increases arterial compliance. The findings in the present study confirm this hypothesis. Reduced bioavailability of endothelium-derived NO impaired compliance, whereas the administration of nitroglycerin, an exogenous NO donor, reversed the loss of compliance induced by L-NMMA.
Elasticity of the arterial wall facilitates healthy behavior of the cardiovascular system. In systole, elasticity reduces left ventricular wall stress by damping the rise in peak systolic pressure.10 The energy thus stored is released in diastole, facilitating organ perfusion throughout the cardiac cycle. A decrease in compliance reduces the diastolic component of blood flow that is particularly important in the coronary arteries and increases the wave reflection from peripheral arteries to accentuate aortic systolic pressure and left ventricular load. Hence, it is perhaps not surprising that loss of arterial elasticity, in its simplest form assessed by widening of arterial pulse pressure, is associated with a marked increase in cardiovascular morbidity and mortality.13–17
Potential Clinical Implications
Cardiovascular risk factors, including hypertension, diabetes, and dyslipidemia, change the composition and thickness of the arterial wall and reduce the bioavailability of constitutive NO.6 Risk factors also reduce arterial compliance and distensibility18–21 as early as the first decade of life, well before structural changes in arteries occur.18 The findings in the present study suggest that the reduction in NO contributes to a loss of arterial elasticity in this setting. While risk factor modification may take years to favorably alter arterial structure, loss of constitutive NO can be corrected more rapidly.6 Thus, future investigations should delineate whether risk factor modification or other therapies directed at improving endothelial vasodilator function can improve arterial elasticity over the same, relatively rapid time course with which they restore NO. In addition, future studies need to define the contribution of NO to elasticity in other arteries, including the aorta.
In conclusion, using a rigorous approach, we have demonstrated that constitutive release of NO contributes to the physiological regulation of elasticity in healthy human brachial arteries in vivo. Future studies should delineate the role of NO in regulating elasticity of other arterial beds and document the effect of risk factor modification on improving arterial elastic properties through augmenting NO.
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Acknowledgments |
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This project was supported by National Institutes of Health grant P50-HL56985. We thank Michael O’Rourke for his comments on this article.
Received January 12, 2001; first decision April 17, 2001; accepted May 22, 2001.
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References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Nichols WW, O’Rourke MF. Therapeutic and monitoring strategies.In: Nichols WW, O’Rourke MF, eds. McDonald’s Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 4th ed. London, UK: Arnold; 1998: 418–438.
2.
O’Rourke M. Arterial stiffness, systolic blood pressure, and logical treatment of arterial hypertension. Hypertension. 1990; 15: 339–347.
3.
Bank AJ, Wilson RF, Kubo SH, Holte JE, Dresing TJ, Wang H. Direct effects of smooth muscle relaxation and contraction on in vivo human brachial artery elastic properties. Circ Res. 1995; 77: 1008–1016.
4.
Bank AJ, Wang H, Holte JE, Mullen K, Shammas R, Kubo SH. Contribution of collagen, elastin, and smooth muscle to in vivo human brachial artery wall stress and elastic modulus. Circulation. 1996; 94: 3263–3270.
5.
Bank AJ, Kaiser DR, Rajala S, Cheng A. In vivo human brachial artery elastic mechanics: effects of smooth muscle relaxation. Circulation. 1999; 100: 41–47.
6. Kinlay S, Selwyn AP, Delagrange D, Creager MA, Libby P, Ganz P. Biological mechanisms for the clinical success of lipid-lowering in coronary artery disease and the use of surrogate end-points. Curr Opin Lipidol. 1996; 7: 389–397.[Medline] [Order article via Infotrieve]
7. Langewouters GJ, Wesseling KH, Goedhard WJ. The static elastic properties of 45 human thoracic and 20 abdominal aortas in vitro and the parameters of a new model. J Biomech. 1984; 17: 425–435.[Medline] [Order article via Infotrieve]
8.
Joannides R, Richard V, Haefeli WE, Benoist A, Linder L, Luscher TF, Thuillez C. Role of nitric oxide in the regulation of the mechanical properties of peripheral conduit arteries in humans. Hypertension. 1997; 30: 1465–1470.
9. Lieberman EH, Gerhard MD, Uehata A, Selwyn AP, Ganz P, Yeung AC, Creager MA. Flow-induced vasodilation of the human brachial artery is impaired in patients <40 years of age with coronary artery disease. Am J Cardiol. 1996; 78: 1210–1214.[Medline] [Order article via Infotrieve]
10. Nichols WW, O’Rourke MF. Properties of the arterial wall: practice.In: Nichols WW, O’Rourke MF, eds. McDonald’s Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 4th ed. London, UK: Arnold; 1998: 73–97.
11. Safar ME, Laurent S, Bouthier JA, London GM. Comparative effects of captopril and isosorbide dinitrate on the arterial wall of hypertensive human brachial arteries. J Cardiovasc Pharmacol. 1986; 8: 1257–1261.[Medline] [Order article via Infotrieve]
12. Safar ME, London GM, Asmar RG, Hugues CJ, Laurent SA. An indirect approach for the study of the elastic modulus of the brachial artery in patients with essential hypertension. Cardiovasc Res. 1986; 20: 563–567.[Medline] [Order article via Infotrieve]
13.
Vaccarino V, Holford TR, Krumholz HM. Pulse pressure and risk for myocardial infarction and heart failure in the elderly. J Am Coll Cardiol. 2000; 36: 130–138.
14. Staessen JA, Gasowski J, Wang JG, Thijs L, Den Hond E, Boissel JP, Coope J, Ekbom T, Gueyffier F, Liu L, Kerlikowske K, Pocock S, Fagard RH. Risks of untreated and treated isolated systolic hypertension in the elderly: meta-analysis of outcome trials. Lancet. 2000; 355: 865–872.[Medline] [Order article via Infotrieve]
15.
Benetos A, Rudnichi A, Safar M, Guize L. Pulse pressure and cardiovascular mortality in normotensive and hypertensive subjects. Hypertension. 1998; 32: 560–564.
16.
Blacher J, Guerin AP, Pannier B, Marchais SJ, Safar ME, London GM. Impact of aortic stiffness on survival in end-stage renal disease. Circulation. 1999; 99: 2434–2439.
17.
Franklin SS, Khan SA, Wong ND, Larson MG, Levy D. Is pulse pressure useful in predicting risk for coronary heart disease? The Framingham Heart Study. Circulation. 1999; 100: 354–360.
18.
Leeson CP, Whincup PH, Cook DG, Mullen MJ, Donald AE, Seymour CA, Deanfield JE. Cholesterol and arterial distensibility in the first decade of life: a population-based study. Circulation. 2000; 101: 1533–1538.
19.
Lehmann ED, Hopkins KD, Rawesh A, Joseph RC, Kongola K, Coppack SW, Gosling RG. Relation between number of cardiovascular risk factors/events and noninvasive Doppler ultrasound assessments of aortic compliance. Hypertension. 1998; 32: 565–569.
20. Taquet A, Bonithon-Kopp C, Simon A, Levenson J, Scarabin Y, Malmejac A, Ducimetiere P, Guize L. Relations of cardiovascular risk factors to aortic pulse wave velocity in asymptomatic middle-aged women. Eur J Epidemiol. 1993; 9: 298–306.[Medline] [Order article via Infotrieve]
21.
Relf IR, Lo CS, Myers KA, Wahlqvist ML. Risk factors for changes in aorto-iliac arterial compliance in healthy men. Arteriosclerosis. 1986; 6: 105–108.
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M. Schmitt, A. Avolio, A. Qasem, C. M. McEniery, M. Butlin, I. B. Wilkinson, and J. R. Cockcroft Basal NO Locally Modulates Human Iliac Artery Function In Vivo Hypertension, July 1, 2005; 46(1): 227 - 231. [Abstract] [Full Text] [PDF]
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 S. J. Williams, D. G. Hemmings, J. M. Mitchell, I. C. McMillen, and S. T. Davidge Effects of maternal hypoxia or nutrient restriction during pregnancy on endothelial function in adult male rat offspring J. Physiol., May 15, 2005; 565(1): 125 - 135. [Abstract] [Full Text] [PDF]
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 S Van Doornum, G McColl, and I P Wicks Atorvastatin reduces arterial stiffness in patients with rheumatoid arthritis Ann Rheum Dis, December 1, 2004; 63(12): 1571 - 1575. [Abstract] [Full Text] [PDF]
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J. Sugawara, S. Maeda, T. Otsuki, T. Tanabe, R. Ajisaka, and M. Matsuda Effects of nitric oxide synthase inhibitor on decrease in peripheral arterial stiffness with acute low-intensity aerobic exercise Am J Physiol Heart Circ Physiol, December 1, 2004; 287(6): H2666 - H2669. [Abstract] [Full Text] [PDF]
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J. A Beckman, R. H Mehta, E. M Isselbacher, E. Bossone, J. V Cooper, D. E Smith, J. Fang, U. Sechtem, L. A Pape, T. Myrmel, et al. Branch vessel complications are increased in aortic dissection patients with renal insufficiency Vascular Medicine, November 1, 2004; 9(4): 267 - 270. [Abstract] [PDF]
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 G. Saliashvili, W. W. Davis, M. T. Harris, N.-A. Le, and W. V. Brown Simvastatin Improved Arterial Compliance in High-Risk Patients Vascular and Endovascular Surgery, November 1, 2004; 38(6): 519 - 523. [Abstract] [PDF]
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M. Schmitt, A. Qasem, C. McEniery, I. B. Wilkinson, V. Tatarinoff, K. Noble, J. Klemes, N. Payne, M. P. Frenneaux, J. Cockcroft, et al. Role of natriuretic peptides in regulation of conduit artery distensibility Am J Physiol Heart Circ Physiol, September 1, 2004; 287(3): H1167 - H1171. [Abstract] [Full Text] [PDF]
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C. M. McEniery, M. Schmitt, A. Qasem, D. J. Webb, A. P. Avolio, I. B. Wilkinson, and J. R. Cockcroft Nebivolol Increases Arterial Distensibility In Vivo Hypertension, September 1, 2004; 44(3): 305 - 310. [Abstract] [Full Text] [PDF]
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I. B. Wilkinson, S. S. Franklin, and J. R. Cockcroft Nitric Oxide and the Regulation of Large Artery Stiffness: From Physiology to Pharmacology Hypertension, August 1, 2004; 44(2): 112 - 116. [Full Text] [PDF]
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 D. K. Ng, K.-L. Kwok, D. Herrington, E. Benjamin, F. J. Nieto, S. Redline, J. Robbins, M. Ip, H.-F. Tse, B. Lam, et al. Endothelial Dysfunction and Sleep Apnea Am. J. Respir. Crit. Care Med., July 15, 2004; 170(2): 197 - 198. [Full Text]
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L. De Angelis, S. C. Millasseau, A. Smith, G. Viberti, R. H. Jones, J. M. Ritter, and P. J. Chowienczyk Sex Differences in Age-Related Stiffening of the Aorta in Subjects With Type 2 Diabetes Hypertension, July 1, 2004; 44(1): 67 - 71. [Abstract] [Full Text] [PDF]
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A. Y. Bagrov and E. G. Lakatta The Dietary Sodium-Blood Pressure Plot "Stiffens" Hypertension, July 1, 2004; 44(1): 22 - 24. [Full Text] [PDF]
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G. Iaccarino, M. Ciccarelli, D. Sorriento, E. Cipolletta, V. Cerullo, G. L. Iovino, A. Paudice, A. Elia, G. Santulli, A. Campanile, et al. AKT Participates in Endothelial Dysfunction in Hypertension Circulation, June 1, 2004; 109(21): 2587 - 2593. [Abstract] [Full Text] [PDF]
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Yasmin, C. M. McEniery, S. Wallace, I. S. Mackenzie, J. R. Cockcroft, and I. B. Wilkinson C-Reactive Protein Is Associated With Arterial Stiffness in Apparently Healthy Individuals Arterioscler Thromb Vasc Biol, May 1, 2004; 24(5): 969 - 974. [Abstract] [Full Text]
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 K. Mather and R. Lewanczuk Measurement of Arterial Stiffness in Diabetes: A cautionary tale Diabetes Care, March 1, 2004; 27(3): 831 - 833. [Full Text] [PDF]
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 J.-B. Liu and B. B. Goldberg Catheter-Based Intraluminal Sonography J. Ultrasound Med., February 1, 2004; 23(2): 145 - 160. [Full Text] [PDF]
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Z. A. Massy, C. Fumeron, D. Borderie, P. Tuppin, T. Nguyen-Khoa, M.-O. Benoit, C. Jacquot, C. Buisson, T. B. Drueke, O. G. Ekindjian, et al. Increased Plasma S-Nitrosothiol Concentrations Predict Cardiovascular Outcomes among Patients with End-Stage Renal Disease: A Prospective Study J. Am. Soc. Nephrol., February 1, 2004; 15(2): 470 - 476. [Abstract] [Full Text] [PDF]
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 C. M. McEniery, A. Qasem, M. Schmitt, A. P. Avolio, J. R. Cockcroft, and I. B. Wilkinson Endothelin-1 regulates arterial pulse wave velocity in vivo J. Am. Coll. Cardiol., December 3, 2003; 42(11): 1975 - 1981. [Abstract] [Full Text] [PDF]
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A. D. Stewart, S. C. Millasseau, M. T. Kearney, J. M. Ritter, and P. J. Chowienczyk Effects of Inhibition of Basal Nitric Oxide Synthesis on Carotid-Femoral Pulse Wave Velocity and Augmentation Index in Humans Hypertension, November 1, 2003; 42(5): 915 - 918. [Abstract] [Full Text] [PDF]
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S. Durier, C. Fassot, S. Laurent, P. Boutouyrie, J.-P. Couetil, E. Fine, P. Lacolley, V. J. Dzau, and R. E. Pratt Physiological Genomics of Human Arteries: Quantitative Relationship Between Gene Expression and Arterial Stiffness Circulation, October 14, 2003; 108(15): 1845 - 1851. [Abstract] [Full Text] [PDF]
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 J. C. Smith, H. Lane, N. Davies, L. M. Evans, J. Cockcroft, M. F. Scanlon, and J. S. Davies The Effects of Depot Long-Acting Somatostatin Analog on Central Aortic Pressure and Arterial Stiffness in Acromegaly J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2556 - 2561. [Abstract] [Full Text] [PDF]
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A. Lerman and J. Herrmann Endothelial function under pressure J. Am. Coll. Cardiol., May 21, 2003; 41(10): 1759 - 1760. [Full Text] [PDF]
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B. N Van Vliet, L. L Chafe, and J.-P. Montani Characteristics of 24 h Telemetered Blood Pressure in eNOS-Knockout and C57Bl/6J Control Mice J. Physiol., May 15, 2003; 549(1): 313 - 325. [Abstract] [Full Text] [PDF]
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J. J. Oliver and D. J. Webb Noninvasive Assessment of Arterial Stiffness and Risk of Atherosclerotic Events Arterioscler Thromb Vasc Biol, April 1, 2003; 23(4): 554 - 566. [Abstract] [Full Text] [PDF]
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K. K. Naka, A. C. Tweddel, D. Parthimos, A. Henderson, J. Goodfellow, and M. P. Frenneaux Arterial distensibility: acute changes following dynamic exercise in normal subjects Am J Physiol Heart Circ Physiol, March 1, 2003; 284(3): H970 - H978. [Abstract] [Full Text] [PDF]
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P. O. Bonetti, L. O. Lerman, and A. Lerman Endothelial Dysfunction: A Marker of Atherosclerotic Risk Arterioscler Thromb Vasc Biol, February 1, 2003; 23(2): 168 - 175. [Abstract] [Full Text] [PDF]
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I. B. Wilkinson, D. J. Webb, J. R. Cockcroft, S. Kinlay, P. Ganz, and M. A. Creager Nitric Oxide and Regulation of Arterial Elasticity: Right Idea, Wrong Vascular Bed? * Response Hypertension, September 1, 2002; e4(3): . [Full Text] [PDF]
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G. F. Mitchell, J. L. Izzo Jr, Y. Lacourciere, J.-P. Ouellet, J. Neutel, C. Qian, L. J. Kerwin, A. J. Block, and M. A. Pfeffer Omapatrilat Reduces Pulse Pressure and Proximal Aortic Stiffness in Patients With Systolic Hypertension: Results of the Conduit Hemodynamics of Omapatrilat International Research Study Circulation, June 25, 2002; 105(25): 2955 - 2961. [Abstract] [Full Text] [PDF]
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I. B. Wilkinson, D. J. Webb, J. R. Cockcroft, S. Kinlay, P. Ganz, and M. A. Creager Nitric Oxide and the Regulation of Arterial Elasticity: Right Idea, Wrong Vascular Bed? Hypertension, April 1, 2002; 39 (4): e26 - e27. [Full Text] [PDF]
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