Acute angiotensin II-mediated restoration of distal renal artery pressure in renal artery stenosis and its relationship to the development of sustained one-kidney hypertension in conscious dogs.

SUMMARY The effects of graded renal artery stenosis on renal and systemic hemodynamics and plasma renin activity (PRA) were studied in conscious, chronically instrumented dogs. In mild and moderate stenosis (following rapid reduction in distal renal artery pressure to 60 or 40 mm Hg) there was initial vasodilatibn followed by prompt restoration within 5-30 minutes of renal artery pressure and vascular resistance; changes in mean aortic pressure (MAP) were minimal. Both A PRA and A renal artery pressure were reciprocally related, the relationship reflecting renal “barostat” control of renin secretion in the conscious dog. Pretreatment with converting enzyme inhibitor before induction of stenosis prevented restoration of renal artery pressure during stenosis. With more severe stenosis, after lowering renal artery pressure to 20 mm Hg, the latter took 2 to 3 days to become fully restored. The MAP rose 18.2 ± 2.5 by the end of 30 minutes but had declined to control by the second or third day. The A PRA during the first hour of stenosis was greater than accounted for by the fall in renal artery pressure, but by Days 2-7 PRA appeared to be predominantly under renal “barostat” control.With even more severe stenosis, systemic MAP remained elevated and after 7 days was 39 ± 14 mm Hg above control levels; PRA also stayed above control levels despite restoration of renal artery pressure, suggesting that it was controlled by factors additional to the “barostat” mechanism. The rise in renal artery pressure was now mainly determined by the increase in systemic MAP. Renal “barostat”-mediated increase in renin-angiotensin activity appears to be the main mechanism that restores renal artery pressure with mild stenosis, while in severe stenosis this is accomplished by development of systemic hypertension.