Endothelium-Derived Nitric Oxide Modulates Vascular Action of Aldosterone in Renal Arteriole

Arima, Shuji; Kohagura, Kentaro; Xu, Hong; Sugawara, Akira; Uruno, Akira; Satoh, Fumitoshi; Takeuchi, Kazuhisa; Ito, Sadayoshi

doi:10.1161/01.hyp.0000111138.78714.1a

Cited by 90 publications

(61 citation statements)

References 42 publications

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“…18 The endothelium may modulate this vasoconstrictor effect by NO release. 19 Aldosterone induced a dose-dependent vasoconstriction in microperfused rabbit afferent arterioles, which was enhanced by disrupting the endothelium. Inhibition of NO synthase induced a similar effect, which was inhibited by chelerythrine, a protein kinase (PKC) inhibitor.…”

Section: Endotheliummentioning

confidence: 98%

Effects of Aldosterone on the Vasculature

2006

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Section: Endotheliummentioning

confidence: 98%

Effects of Aldosterone on the Vasculature

2006

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“…Arima et al 64 reported that aldosterone can activate NOS 3 in renal arterioles, leading to NO production; however, the mechanism involved was not investigated. Taylor et al 65 found that in ET B receptor-deficient rats, medullary NOS activity and renal endothelin production are decreased, indicating that renal endothelin regulates NOS 3 activity as reported for the thick ascending limb.…”

Section: Hormonal Regulation Of Nosmentioning

confidence: 99%

Recent Advances in the Regulation of Nitric Oxide in the Kidney

Herrera

Garvin

2005

Hypertension

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Abstract-Nitric oxide (NO) plays important roles in the regulation of renal function and the long-term control of blood pressure. New roles of NO have been proposed recently in diabetes, nephrotoxicity, and pregnancy. NO derived from all 3 NOS isoforms contributes to the overall regulation of kidney function, and recent advances in our understanding of their regulation have been made lately. In this regard, substrate and cofactor availability play important roles in regulating nitric oxide synthase (NOS) activity not only by limiting enzyme activity but also by influencing the coupling of NOS with its cofactors, tetrahydrobiopterin and NADPH. Protein-protein interactions are now recognized to be important negative and positive regulators of NOS. Phosphorylation is another component of the mechanism whereby NOS is activated or deactivated. Increased NOS expression can also influence enzyme activity; however, the degree of expression does not always correlate with enzyme activity because increased NO levels can result in inhibition of NOS. Finally, other potential regulators of NOS such as endogenous L-arginine analogs may also be important. In this article, we summarize recent advances in the regulation of activity and expression of the NOS isoforms within the kidney. renal function and long-term regulation of blood pressure. [1][2][3][4] This is best evidenced by the fact that inhibiting intrarenal NO production increased blood pressure. 5 In addition, reduced NO has been identified as a common denominator of many hypertensive models. 6 -9 The effects of NO on blood pressure via actions in the kidney occur through multiple mechanisms. These include increasing renal blood flow caused by vasodilatation, 10 increasing glomerular filtration, 11 inhibiting sodium transport along the nephron, 12-14 and regulating release of renin. 15 NO produced by each of the 3 nitric oxide synthases (NOS), NOS 1, NOS 2, and NOS 3, reportedly contributes to the regulation of renal function. Inhibition of NOS activity within the kidney is known to lead to sodium retention and hypertension. This review addresses recent advances in our understanding of the role played by renal NO in various physiological and pathophysiological conditions, as well as how NO production is regulated. Roles for Renal NOHistorically, NO produced by the kidney has been thought of primarily as a factor that regulates urinary volume and sodium excretion. The physiological effects of NO can be mediated via changes in renal hemodynamics and/or salt and water absorption by the nephron. NO reduces renal vascular tone in part by dilating the afferent arteriole. 16 It also increases glomerular filtration rate. 11 NO modulates renin secretion by the juxtaglomerular apparatus 15 and tubuloglomerular feedback. 3 Finally, NO regulates transport in various nephron segments as reviewed recently by Ortiz and Garvin. 12 More recently it has been recognized that in a number of pathophysiological conditions, the actions of NO on renal hemodynamics and/or nephron transport are ...

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“…However, substantial evidence has emerged to show that aldosterone also plays an independent role in mediating cardiovascular damage. It plays a major role in cardiac and vascular remodelling, regulating collagen turnover and fibrous tissue formation, though some evidence suggests that it may have short-term vascular effects, leading to vasoconstriction in both in vitro studies 29 and in vivo in man. 30,31 Long-term increases in aldosterone lead to deleterious effects on the vascular matrix, by increasing collagen content and fibrosis.…”

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confidence: 99%

Review: Arterial stiffness and the renin-angiotensin-aldosterone system

Mahmud

Feely

2004

J Renin Angiotensin Aldosterone Syst

113

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Arterial stiffness has recently been recognised as an independent risk factor for cardiovascular morbidity and mortality in hypertension. Many of the complications seen with angiotensin II (Ang II) excess or hyperaldosteronism -an increased event rate, left ventricular hypertrophy, endothelial dysfunction and target organ damage -are also associated with arterial stiffness. It is possible that reduced arterial compliance may be one mechanism whereby increased activity of the renin-angiotensin-aldosterone system (RAAS) produces adverse vascular effects. Common pathophysiological processes, altered collagen turnover and increased fibrosis may underlie both arterial stiffness and RAAS-associated vascular damage.While it is recognised that patients with hyperaldosteronism have increased arterial stiffness, the role of the RAAS in modulating arterial compliance in essential hypertension and in normotensive subjects is less clear cut. There is, however, more consistent data which show that drugs that interfere with Ang II or aldosterone, namely angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) and aldosterone antagonists, all reduce arterial stiffness. In many cases, this is to a greater extent than predicted from the extent of reduction in blood pressure (BP), suggesting a role for RAAS in vascular stiffness in hypertensive subjects. There is also evidence that combined ACE inhibitors (ACE-Is) and ARBs may have an additive effect in reducing stiffness. The reduction in cardiovascular mortality in end-stage renal disease patients treated with ACE-Is was preferentially seen in those who had reduced arterial stiffness. These data suggest that, in addition to regulation of vascular biology and BP, the RAAS is an important determinant of arterial stiffness in health and, more particularly, in disease. IntroductionThe pulse has retained a central role throughout the history of medicine. It was, however, more an art than a science until the 19th century, when sphygmography provided the first graphic recordings of the arterial pressure pulse. Abnormalities in the pulse wave contour were considered indicative of stiff arteries and subsequently used to diagnose hypertension and Bright's disease.About the same time as Tigerstedt and Bergman discovered renin, sphygmography was abandoned in favour of cuff sphygmomanometry. There has been a recent awakening in the field of arterial stiffness follow-

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Endothelium-Derived Nitric Oxide Modulates Vascular Action of Aldosterone in Renal Arteriole

Cited by 90 publications

References 42 publications

Effects of Aldosterone on the Vasculature

Effects of Aldosterone on the Vasculature

Recent Advances in the Regulation of Nitric Oxide in the Kidney

Review: Arterial stiffness and the renin-angiotensin-aldosterone system

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