Angiotensin-(1–7)–Induced Renal Vasodilation in Hypertensive Humans Is Attenuated by Low Sodium Intake and Angiotensin II Co-InfusionNovelty and Significance

摘要

Current evidence suggests that angiotensin-(1–7) plays an important role in the regulation of tissue blood flow. This evidence, however, is restricted to studies in animals and human forearm. Therefore, we studied the effects of intrarenal angiotensin-(1–7) infusion on renal blood flow in hypertensive humans. To assess the influence of renin–angiotensin system activity, sodium intake was varied and co-infusion with angiotensin II was performed in a subgroup. In 57 hypertensive patients who were scheduled for renal angiography, renal blood flow was measured (133Xenon washout method) before and during intrarenal infusion of angiotensin-(1–7) (3 incremental doses: 0.27, 0.9, and 2.7 ng/kg per minute). Patients were randomized into low or high sodium intake. These 2 groups of patients received angiotensin-(1–7), with or without intrarenal co-infusion of angiotensin II (0.3 ng/kg per minute). Angiotensin-(1–7) infusion resulted in intrarenal vasodilation in patients adhering to a sodium-rich diet. This vasodilatory effect of angiotensin-(1–7) was clearly attenuated by low sodium intake, angiotensin II co-infusion, or both. Regression analyses showed that the prevailing renin concentration was the only independent predictor of angiotensin-(1–7)–induced renal vasodilation. In conclusion, angiotensin-(1–7) induces renal vasodilation in hypertensive humans, but the effect of angiotensin-(1–7) is clearly attenuated by low sodium intake and co-infusion of angiotensin II. This supports the hypothesis that angiotensin-(1–7) induced renal vasodilation depends on the degree of renin-angiotensin-system activation.