Key result
Angiotensin-(1-7)-induced renal vasodilation was significantly reduced in stenotic kidneys compared to essentially hypertensive controls, but preserved in contralateral nonstenotic kidneys.
Why the study?
Does local infusion of angiotensin-(1-7) increase renal blood flow in hypertensive patients with atherosclerotic renal artery stenosis compared to controls?
Observational
Does local infusion of angiotensin-(1-7) increase renal blood flow in hypertensive patients with atherosclerotic renal artery stenosis compared to controls?
The vasodilatory effect of angiotensin-(1-7) is blunted in kidneys with atherosclerotic renal artery stenosis, suggesting local altered blood flow regulation rather than a generalized atherosclerotic effect.
Answers are grounded in this paper and cite their sources.
Ang-(1-7) vasodilation appears blunted locally in stenotic kidneys; hypothesis-generating for RAS effects in ARAS, prospective studies needed.
BACKGROUND: Angiotensin-(1-7) modulates renal blood flow in humans with essential hypertension by inducing vasodilation and counterbalancing angiotensin II-induced vasoconstriction. Little is, however, known about the effects of angiotensin-(1-7) in kidneys with atherosclerotic renal artery stenosis. We previously demonstrated that the effect of angiotensin-(1-7) is reduced in patients with increased activity of the renin-angiotensin system. As the renin-angiotensin system is also activated in kidneys with renal artery stenosis, we hypothesized that the vasodilatory effect of angiotensin-(1-7) is also reduced in such kidneys. METHOD: Therefore, we selectively measured mean renal blood flow (¹³³Xenon washout method) before and during local infusion of angiotensin-(1-7) (0.27, 0.9, and 2.7 ng/kg per min) in hypertensive patients who were angiographically evaluated for the presence of renovascular abnormalities. Data were analyzed in three groups: stenotic kidneys, nonstenotic kidneys with renal artery stenosis of the contralateral kidney (contralateral stenotic kidneys), or essentially hypertensive controls without renovascular abnormalities (matched for urinary sodium excretion). RESULTS: Angiotensin-(1-7) infusion resulted in an increase in renal blood flow in matched controls. In stenotic kidneys however, the effect of angiotensin-(1-7) was significantly reduced as compared to controls. The angiotensin-(1-7) effect in contralateral stenotic kidneys was comparable to controls. CONCLUSION: Angiotensin-(1-7)-induced vasodilation is reduced in stenotic kidneys, but not in contralateral stenotic kidneys. This suggests that the altered blood flow regulation in kidneys with atherosclerotic renal artery stenosis is a local phenomenon and not related to generalized atherosclerotic burden. Probably, the renin-angiotensin system activation, bioavailability of nitric oxide, and structural changes in the stenotic kidney play a role in this phenomenon.
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Twist et al. (2014) conducted an observational in Hypertension with or without renal artery stenosis. Angiotensin-(1-7) infusion vs. Essentially hypertensive controls was evaluated on Mean renal blood flow. Angiotensin-(1-7)-induced renal vasodilation was significantly reduced in stenotic kidneys compared to essentially hypertensive controls, but preserved in contralateral nonstenotic kidneys.
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