Prostaglandins in the beta-adrenergic and baroreceptor-mediated secretion of renin

Abstract

Prostaglandins (PG) play a central role in the control of renin secretion. The participation of PG in .beta.-adrenergic and baroreceptor-mediated release of renin was determined. The effect of i.v. isoproterenol (ISO) (0.018 .mu.g/kg per min) on renin activity was examined in anesthetized dogs before and after PG inhibition with indomethacin (10 mg/kg). Before PG inhibition isoproterenol increased plasma renin activity (PRA) from 3.2 .+-. 1.3 to 15.6 .+-. 3.4 ng angiotensin I (AI)/ml per h (P < 0.001), while after PG inhibition isoproterenol increased PRA to the same degree from 4.8 .+-. 1.7 to 14.2 .+-. 3.2 ng AI/ml per h (P < 0.005). Since isoproterenol also decreased systemic and renal perfusion pressure both before and after indomethacin, the possibility was examined that the increase in PRA during PG inhibition was mediated by the decrease in renal perfusion pressure. Administration of isoproterenol in dogs with controlled renal perfusion pressure increased PRA in the absence (from 11.7 .+-. 2.9 to 23.8 .+-. 4.7 ng AI/ml per h, P < 0.001) and presence (from 8.6 .+-. 2.3 to 18.9 .+-. 5.0 ng AI/ml per h, P < 0.05) of PG inhibition. Before PG inhibition a decrease in renal perfusion pressure by 30-40 mmHg increased PRA from 6.3 .+-. 1.6 to 11.2 .+-. 2.5 ng AI/ml per h (P < 0.01). After PG inhibition the same degree of aortic constriction failed to cause renin release as PRA remained essentially unchanged (4.5 .+-. 1.4 and 4.0 .+-. 1.2 ng AI/ml per h). The renin stimulatory effect of .beta.-adrenergic stimulation is evidently not impaired by inhibition of PG synthesis, but baroreceptor stimulation of renin apparently requires normal PG synthesis.