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

more »

... 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. (Hypertension 1: 292- 298, 1979) KEY WORDS • critical stenosis renin • renal blood flow • renal hemodynamics renal hypertension • renal barostat R ECENT theoretical and experimental analysis has shown that the pressure gradient across a fixed diameter stenosis is not a linear function of flow, as it is for Poiseuille's relationship. 1 ' 2 Young and colleagues 1 have suggested that an appropriate hydraulic model is a nonlinear stenosis resistance in series with the resistance of the distal vascular bed. To achieve a given pressure drop experimentally across a stenosis, a greater reduction in vessel diameter will be required when the distal vascular bed is constricted than when it is dilated. l~*