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In normotensive subjects, acute reduction of mean arterial pressure to from 60 to 75 mm Hg by infusion of sodium nitroprusside caused significant increase in renin activity of renal venous plasma and also in the renal-systemic difference of renin activity. At the same time, the products of the renal-systemic difference of renin activity and renal plasma flow increased significantly, whereas renin substrate activity of plasma was unchanged, indicating that there was an increase in renin release during reduction in pressure. Renin activity of renal venous plasma, expressed in logarithms, showed a significant correlation with the degree of reduction in pressure; an increase in renin activity became significant when mean arterial pressure was reduced to below a level of 70 to 75 mm Hg. There was a striking difference in the renal response to reduction in pressure between patients with renovascular hypertension and normotensive subjects. In 10 renovascular hypertensive patients, significant increase in renin release occurred from the involved kidney at mean arterial pressures ranging from 90 to 137 mm Hg; the threshold at which renin release increased was shifted to a range much higher than that in normotensive subjects. Furthermore, the magnitude of renin release from the involved kidney was significantly greater when compared to that in normotensive subjects. In contrast, in the contralateral uninvolved kidney, no significant release of renin was detected during reduction in pressure. The renal mechanism controlling renin secretion appears to be operative at higher systemic arterial pressure levels and with enhanced responsiveness in the involved kidney of renovascular hypertensive patients; the findings are consistent with the hypothesis that the renin-angiotensin system participates in maintaining hypertension in this disease.
Kaneko et al. (Mon,) studied this question.