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Effects of Angiotensin-(1-7) on Forearm Circulation in Normotensive Subjects and Patients With Essential Hypertension
Author(s) -
Shota Sasaki,
Yukihito Higashi,
Keigo Nakagawa,
Hideo Matsuura,
Goro Kajiyama,
Tetsuya Oshima
Publication year - 2001
Publication title -
hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.986
H-Index - 265
eISSN - 1524-4563
pISSN - 0194-911X
DOI - 10.1161/01.hyp.38.1.90
Subject(s) - forearm , essential hypertension , medicine , angiotensin ii , cardiology , circulation (fluid dynamics) , pathophysiology of hypertension , blood pressure , renin–angiotensin system , endocrinology , surgery , physics , thermodynamics
Previous animal studies have shown that angiotensin (Ang)-(1-7) is a biologically active component of the renin-angiotensin system, acting as a vasoactive agent, and may play a role in the blood pressure regulation. There is little information, however, on the effect of Ang-(1-7) on human circulation or the mechanism of its action. To investigate the effect of Ang-(1-7) on forearm circulation and to determine whether this effect is altered in patients with essential hypertension, we measured change in forearm blood flow using venous occlusion plethysmography in response to intra-arterial infusion of Ang-(1-7) (10(-10), 10(-9), and 10(-8) mol/min; for 5 minutes) in normotensive control subjects (n=8) and patients with essential hypertension (n=8). Infusion of Ang-(1-7) significantly increased the forearm blood flow response in a dose-dependent manner in both normotensive control subjects (28.7+/-9.7%, at 10(-8) mol/min; P<0.05) and hypertensive patients (31.8+/-15.2%, at 10(-8) mol/min; P<0.05). The vasodilatory effect of Ang-(1-7) was similar in the two groups. Intra-arterial infusion of N(G)-monomethyl-L-arginine, a nitric oxide synthesis inhibitor, did not alter the forearm blood flow response to Ang-(1-7) in either group. These findings suggest that Ang-(1-7) causes vasodilation in forearm circulation of normotensive subjects and patients with essential hypertension through a pathway that is independent of nitric oxide synthesis.

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