(Hypertension. 2001;38:90.)
© 2001 American Heart Association, Inc.
Scientific Contributions |
From the First Department of Internal Medicine (S.S., Y.H., K.N., H.M., G.K.) and the Department of Clinical Laboratory Medicine (T.O.), Hiroshima University School of Medicine, Japan.
Correspondence to Shota Sasaki, MD, Hiroshima University School of Medicine, First Department of Internal Medicine, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan. E-mail sshota{at}mcai.med.hiroshima-u.ac.jp
Abstract 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 NG-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.
Key Words: angiotensin-(1-7) forearm blood flow nitric oxide hypertension, essential
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