@EN To determine to effect of angiotensin II (ANG II)-induced hypertension on the renovarcular respones to norepinephrine (NE), six anesthetized dogs instrumented for monitoring of renal blood flow (RBF) were subjected to step increases every 2
minutes
in the rate of norepinephrine infusion into the renal artery during 1) control conditions (C), 2) servocontrol of renal arterial pressure (RAP) at levels expected to be achieved during acute captopril administration(C+S), 3) acute captopril
administration (CEI), 4) angiotensin II infusion simultaneously with captopril at concentrations which restored RAP toward control (CEI+A), and 5) servocontrol of RAP during captoprii and angiotensin II4) angiotensin II infusion simultaneously
with
captopril at concentrations which restored RAP (SEI+A+S). Whether the plasma levels of ANG II were allowed to increase (C, C+S) or not (CEI+A, CEI+A+S) with NE infusion, there were no differences in RBF response to NE infusion between C and C+S
and
between CEI+A and CEI+A+S, which implies that , RAP does not play an important role in modulating the renovascular response to NE. However. When. Captopril was administered without ANG II replacement (CEI), RBF induced severe renal ischemia at
much
lower rates of NE infusion than occurred when the sufficient concentration of ANG II were present in the plasma.
Since this enhanced sensitivity to NE did not occur at RAP's lower than those achieved during acute captopril administration once ANG II was present in the plasma in sufficient concentrations, it is likely that ANG II exerts a protective effect
on
the
kidney during renal adrenergic stimulation through a mechanism other than increasing systemic arterial pressure.
|