Endothelium-dependent mechanical properties of the carotid artery in WKY and SHR. Role of angiotensin converting enzyme inhibition.

Lévy, Bernard; Benessiano, J; Poitevin, Pierre; Safar, Michel E.

doi:10.1161/01.res.66.2.321

Cited by 95 publications

(69 citation statements)

References 35 publications

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“…Structural components within the arterial wall, mainly collagen and elastin, together with transmural pressure, are key determinants of large vessel stiffness. However, smooth muscle tone also influences the stiffness of elastic and muscular arteries, suggesting functional regulation of stiffness by local and/or circulating vasoactive substances (32)(33)(34). Indeed, we and other investigators have recently demonstrated in both animals (7) and humans (8,9) that one important regulatory molecule is endothelial-derived NO.…”

Section: Discussionmentioning

confidence: 98%

Inflammation and arterial stiffness in systemic vasculitis: A model of vascular inflammation

Booth¹,

Wallace²,

McEniery³

et al. 2004

Arthritis & Rheumatism

217

122

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Objective. Arterial stiffness, an independent determinant of cardiovascular risk, is regulated by both structural and functional factors, including endothelium-derived nitric oxide. Endothelial dysfunction is associated with acute and chronic systemic inflammation. However, the role of systemic inflammation in arterial stiffening has not been determined. The aim of this study was to investigate the relationship between inflammation and arterial stiffness in patients with antineutrophil cytoplasmic antibody-associated systemic vasculitis (AASV) as a model of systemic inflammation.Methods. Thirty-one patients with AASV (15 with active disease) and 32 age-matched controls were studied. Pulse wave velocity (PWV) and the augmentation index (AIx) were assessed noninvasively and related to serum levels of C-reactive protein (CRP), interleukin-6, and tumor necrosis factor ␣.Results. In subjects with active disease, the AIx, PWV, and level of CRP were elevated compared with that in controls (mean ؎ SEM 31 ؎ 3% versus 22 Conclusion. These data indicate that AASV is associated with increased arterial stiffness, and that stiffness correlates with the degree of active inflammation.

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Section: Discussionmentioning

confidence: 98%

Inflammation and arterial stiffness in systemic vasculitis: A model of vascular inflammation

Booth¹,

Wallace²,

McEniery³

et al. 2004

Arthritis & Rheumatism

217

122

View full text Add to dashboard Cite

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“…The reasons remain to be defined (45,54); however, vascular myogenic responses have been implicated in the generation and buffering of LF BP fluctuations (1,24,60,66). Of particular relevance, parallel differences between ANG II and PE were observed with respect to the fractional gain of the myogenic response in the renal transfer function data (see Table 2).…”

Section: Discussionmentioning

confidence: 98%

Blood pressure-renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats

Polichnowski

Griffin

Long

et al. 2013

American Journal of Physiology-Renal Physiology

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Polichnowski AJ, Griffin KA, Long J, Williamson GA, Bidani AK. Blood pressure-renal blood flow relationships in conscious angiotensin II-and phenylephrine-infused rats. Am J Physiol Renal Physiol 305: F1074 -F1084, 2013. First published July 3, 2013 doi:10.1152/ajprenal.00111.2013.-Chronic ANG II infusion in rodents is widely used as an experimental model of hypertension, yet very limited data are available describing the resulting blood pressurerenal blood flow (BP-RBF) relationships in conscious rats. Accordingly, male Sprague-Dawley rats (n ϭ 19) were instrumented for chronic measurements of BP (radiotelemetry) and RBF (Transonic Systems, Ithaca, NY). One week later, two or three separate 2-h recordings of BP and RBF were obtained in conscious rats at 24-h intervals, in addition to separate 24-h BP recordings. Rats were then administered either ANG II (n ϭ 11, 125 ng·kg Ϫ1 ·min Ϫ1 ) or phenylephrine (PE; n ϭ 8, 50 mg·kg Ϫ1 ·day Ϫ1 ) as a control, ANG IIindependent, pressor agent. Three days later the BP-RBF and 24-h BP recordings were repeated over several days. Despite similar increases in BP, PE led to significantly greater BP lability at the heart beat and very low frequency bandwidths. Conversely, ANG II, but not PE, caused significant renal vasoconstriction (a 62% increase in renal vascular resistance and a 21% decrease in RBF) and increased variability in BP-RBF relationships. Transfer function analysis of BP (input) and RBF (output) were consistent with a significant potentiation of the renal myogenic mechanism during ANG II administration, likely contributing, in part, to the exaggerated reductions in RBF during periods of BP elevations. We conclude that relatively equipressor doses of ANG II and PE lead to greatly different ambient BP profiles and effects on the renal vasculature when assessed in conscious rats. These data may have important implications regarding the pathogenesis of hypertension-induced injury in these models of hypertension.hypertension; hemodynamics; blood pressure variability INCREASED ACTIVITY OF THE renin-angiotensin-aldosterone system (RAAS) (40,56,73) is postulated to be a major contributor to chronic kidney disease progression through both blood pressure (BP)-dependent and -independent mechanisms (7,28,39,73). Accordingly, chronic ANG II infusion is extensively used to investigate mechanisms that mediate renal damage in hypertensive states characterized by enhanced RAAS activation (3,20,42,65,71). Renal parenchymal injury with significant tubulointerstitial fibrosis and a propensity to develop salt-sensitive hypertension has been observed after ANG II infusions (44, 57). Both barotrauma and renal vasoconstrictionmediated tissue ischemia have been postulated to initiate the pathogenic cascades that lead to renal injury after chronic ANG II infusions. However, despite its wide use, there is a paucity of experimental data describing the BP-renal blood flow (RBF) relationships in conscious ANG II-infused animals, and the relative contribution of these two initiating mechanisms ...

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“…16 These findings suggested that endothelium function and arterial stiffness are causally associated and that a contribution of vasoconstrictive substances is required for this process, with more pronounced diameter and compliance enhancement in normotensive control rats than in SHR. 16 On the other hand, when the radial artery of normotensive humans is studied in vivo, NOS inhibition did not change arterial caliber but increased arterial compliance, an observation supporting the presence of compensating vasodilation mechanisms. 19 Taken together, such findings suggest that the balance of vasodilating and vasoconstricting effectors of the endothelium have different effects in SHR and WKY.…”

Section: Thoracic Aortas and Carotid Arteries In Young Shrmentioning

confidence: 89%

Pulse Pressure, Endothelium Function, and Arterial Stiffness in Spontaneously Hypertensive Rats

et al. 2001

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Abstract-In rats, removal of the carotid arterial or abdominal aortic endothelium results in an acute increase of diameter and compliance. In humans, acute local administration of a specific NO synthase inhibitor increases radial artery compliance but not the diameter. The purpose of this review is to determine whether in spontaneously hypertensive rats (SHR), a cause-and-effect relationship may be observed between endothelial function and arterial stiffness with possible consequences on pulse pressure (PP) control. The study is based on a comparative time-dependent analysis of the following in young and old SHR: aortic blood pressure measurements and reactivity, ultrasonographic arterial stiffness assessment, aortic histomorphometry and staining, and molecular biology with evaluation of endothelium function. In young SHR, aortic mean blood pressure and PP increase proportionally, whereas isobaric arterial stiffness is unchanged or poorly modified. The endothelial NO response to norepinephrine is normal or upregulated as a response to predominant vasoconstrictive influences. In contrast, in old SHR, PP and mean blood pressure change disproportionately with age, together with an enhanced isobaric arterial stiffness. The endothelial NO response to norepinephrine is abolished, in association with endothelium-dependent heightened norepinephrine reactivity and enhanced accumulation of vessel extracellular matrix. In this latter case, exogenous NO acutely and selectively lowers the increased PP. Thus, during SHR aging, a negative feedback may be observed between NO bioactivity and PP through changes in arterial structure and function. Whether this alteration contributes to the development of systolic hypertension in old populations remains to be determined. Key Words: rats, inbred SHR Ⅲ arteries Ⅲ endothelium Ⅲ nitric oxide F or many years, studies of spontaneous hypertension in rats focused on the presence of sympathetic hyperactivity and the mechanisms by which this alteration contributes to changing the mean blood pressure (MBP) and the structure and function of arterioles. 1,2 Subsequently, the role of the vascular endothelium was principally deduced from the investigation of NO-norepinephrine (NE) interactions. 3 Nowadays, hypertension is mainly considered as a cardiovascular risk factor, leading to more attention being focused on the structure and function of hypertensive large arteries, which greatly influence the development of complications in hypertensive vascular disease. 4 It has been widely reported that the conduit arteries of spontaneously hypertensive rats (SHR) are stiffer than those of the corresponding normotensive control rats. 4,5 In addition to blood pressure level, it seems likely that intrinsic modifications of the arterial wall might contribute to the increased stiffness. 4 Because stiffness is influenced by arterial structure and function, changes in vasomotor tone, possibly of endothelial origin, might promote the alterations of the mechanical properties of the SHR conduit arteries.The purpo...

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Endothelium-dependent mechanical properties of the carotid artery in WKY and SHR. Role of angiotensin converting enzyme inhibition.

Cited by 95 publications

References 35 publications

Inflammation and arterial stiffness in systemic vasculitis: A model of vascular inflammation

Inflammation and arterial stiffness in systemic vasculitis: A model of vascular inflammation

Blood pressure-renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats

Pulse Pressure, Endothelium Function, and Arterial Stiffness in Spontaneously Hypertensive Rats

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