(Hypertension. 1995;25:796-802.)
© 1995 American Heart Association, Inc.
Articles |
Angiotensin-(1-7) and Nitric Oxide Interaction in Renovascular Hypertension
From the Hypertension Center and the Department of General Surgery, The Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, NC.
Correspondence to Carlos M. Ferrario, MD, Hypertension Center, Bowman Gray School of Medicine of Wake Forest University, Medical Center Blvd, Winston-Salem, NC 27157-1032.
Abstract New studies suggest that vasodilator systems
may play an important role in restraining the rise in peripheral
vascular resistance associated with the evolution of arterial
hypertension. We characterized in conscious dogs the hemodynamic and
hormonal effects of 4 weeks of feeding either the nitric oxide synthase
inhibitor N
-nitro-L-arginine (3
mg · kg-1 · d-1) or the nitric oxide
precursor L-arginine (0.3
mg · kg-1 · d-1) during the evolution
of two-kidney, one clip hypertension. Inhibition of nitric oxide
production elicited a form of hypertension more severe than that
produced in placebo-fed two-kidney, one clip dogs. The higher levels of
blood pressure were accompanied by lower levels of plasma renin
activity and lower angiotensin II concentrations. During the chronic
phase of renovascular hypertension, the fall in blood pressure produced
by acute systemic injections of lisinopril or losartan was
significantly reduced in dogs given the nitric oxide inhibitor. In
contrast, chronic administration of L-arginine had no
effect on the magnitude of hypertension or on the increases in renin
activity and hyperangiotensinemia associated with the evolution of
renal hypertension. Likewise, the fall in blood pressure produced by
pharmacological blockade of angiotensin II was not different from that
recorded in untreated renal hypertensive dogs. The vasodilator
component of the blood pressure response due to intravenous injections
of angiotensin-(1-7) (1 to 100 nmol/kg) was augmented in both untreated
and L-arginine–treated two-kidney, one clip hypertensive
dogs, but was significantly attenuated in hypertensive dogs fed the
nitric oxide synthase inhibitor. These experiments demonstrated an
important contribution of nitric oxide in modulating the increased
activity of the peripheral renin-angiotensin system during the
evolution of renovascular hypertension. Furthermore, our data show that
the evolution of this form of experimental renal hypertension is
accompanied by a magnification of the vasodilator actions of
angiotensin-(1-7). Activation of endothelium-derived relaxing factors
and angiotensin-(1-7) mechanisms may act in synergy to buffer the
increase in vascular resistance produced by chronic renal ischemia.
Key Words: angiotensins • angiotensin II • losartan • hypertension, renal • nitric oxide • vascular resistance
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