Pressor responses to norepinephrine during captopril in renal prehypertensive rabbits.

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Abstract
The role of angiotensin II (AII) in pressor hyperresponsiveness was examined in conscious 1-kidney, 1 clip rabbits with renal artery stenosis on 3-days'' duration (renal prehypertensive rabbits). Conscious 1-kidney rabbits without renal artery stenosis served as controls. Two experiments were performed. The 1st experiment used 4 groups of 6 rabbits each, to examine the pressor responses to i.v. infusions of norepinephrine (NE) 25-1200 ng/min per kg body weight, in 3-day renal artery stenosis and in 3-day control rabbits, receiving NE plus the angiotensin-converting enzyme inhibitor, captopril (SQ 14,225), or receiving NE alone. The arterial pressure and values for plasma renin activity (PRA) were the same in the renal artery stenosis rabbits as in the controls. The exaggerated pressor responses to NE in the renal artery stenosis rabbits were restored to normal by captopril administration. The 2nd experiment investigated the pressor responses to i.v. infusions of NE 800 ng/min per kg in 6 rabbits with renal artery stenosis and in 6 control rabbits before captopril, during captopril administration, and during the administration of captopril plus the i.v. infusion of AII at 0.5, 1.0, and 2.0 ng/min/kg body weight. Plasma concentrations of AII were determined at each point in this experiment. The renal artery stenosis rabbits had the same values for arterial pressure and PRA as the control rabbits. The renal artery stenosis rabbits had increased pressor responses to NE, and this pressor hyperresponsiveness was abolished by captopril. The i.v. infusion of AII during captopril treatment in the renal artery stenosis rabbits increased the pressor responses to NE, and AII 2.0 ng/min per kg completely restored the pressor hyperresponsiveness in these rabbits. The control rabbits had no changes in the pressor responses to NE with captopril or with captopril plus any of the AII doses. Before captopril, the control and renal artery stenosis rabbits had the same plasma concentrations of AII. With captopril, plasma concentrations of AII in the renal artery stenosis rabbits decreased to undetectably low levels and remained so during the infusions of AII at all doses. Evidently plasma AII plays an important role in the enhanced pressor responses to NE in 3-day renal artery stenosis rabbits, and this effect is not due to elevated plasma levels of AII.