The purpose of this study was to determine whether the sensitivity of the renal vasculautre to norepinephrine depends on the renal perfusion pressure.
In pentobarbital-anesthetized dogs with suprarenal aortic occluder and electromagnetic flow probes...
The purpose of this study was to determine whether the sensitivity of the renal vasculautre to norepinephrine depends on the renal perfusion pressure.
In pentobarbital-anesthetized dogs with suprarenal aortic occluder and electromagnetic flow probes around the renal artery, renal blood flow (RBF), renal arterial pressure (RAP), and mean arterial pressure (MAP) were measured 1) during control condition in which RAP was allowed to change during norepinephrine (NE) infusion, 2) when RAP was maintained constant at NE-preinfusion levels, and 3) when RAP was maintained at levels where autoregulation of RBF no longer occurs.
During control condition, NE (0.3㎍/kg/min) increased MAP from 119±3 to 123±4 mmHg and renal resistance (RR) from 0.569±0.048 to 0.593±0.056 mmHg.min/ml. There was no significant change in RBF. The maintenance of RAP at preinfusion level prevented RR from increasing during NE infusion. However, when RPP was reduced to and maintained at RAP below which autoregulation no longer occurs (70±2ml), NE infusion decreased RBF and increased RR.
These data indicate that the local autoregulation of the kidney affects vascular resistance during NE-induced hypertension, and that the enhanced sensitivity of renal vasculature to NE at RAP below the autoregulatory limit is likely to be due to the lack of tubuloglomerular feedback-mediated vasodilation at the low pressure levels.