Key result
Chronic intrarenal AngII infusion fails to alter canine renal blood flow responses or induce vascular hypertrophy.
Why the study?
It was uncertain whether chronic intrarenal angiotensin II infusion alters renal vascular responsiveness to vasoactive agents, indicating possible vascular structural changes.
Does chronic intrarenal AngII infusion alter renal vascular responsiveness to vasoactive agents in conscious dogs?
Does chronic intrarenal AngII infusion alter renal vascular responsiveness to vasoactive agents in conscious dogs?
Chronic intrarenal AngII infusion does not alter renal vascular responsiveness to vasoactive agents, providing no evidence for renal vascular hypertrophy in conscious dogs.
No support for AngII-induced renal hypertrophy in conscious dogs; leaves open its role in human renovascular disease.
We tested whether chronic intrarenal angiotensin II (AngII) infusion altered renal vascular responsiveness to vasoactive agents, which would provide evidence of vascular structural changes. 2. The renal blood flow (RBF) responses to renal arterial administration of bolus doses of acetylcholine, glyceryl trinitrate, AngII and noradrenaline were measured before commencement of and 1 day after cessation of 28 days intrarenal AngII infusion (0.5 ng/kg per min) in chronically instrumented conscious dogs. 3. The RBF responses to these vasoactive agents were unaltered by chronic intrarenal AngII infusion in conscious dogs. 4. These functional studies provide no evidence for renal vascular hypertrophy in response to chronic intrarenal AngII infusion in conscious dogs.
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Fitzgerald et al. (1998) studied this question. Intrarenal angiotensin II (AngII) infusion vs. Baseline (before commencement of infusion) was evaluated on Renal blood flow (RBF) responses to renal arterial administration of bolus doses of acetylcholine, glyceryl trinitrate, AngII and noradrenaline. Chronic intrarenal AngII infusion for 28 days did not alter renal blood flow responses to vasoactive agents in conscious dogs, providing no evidence for renal vascular hypertrophy.
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