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

Prostaglandins (PG) play a central role in the control of renin secretion. These studies were undertaken to determine the participation of PG in beta-adrenergic and baroreceptor-mediated release of renin. The effect of intravenous isoproterenol (ISO) (0.018 μg/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. However, 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). However, 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). These results strongly suggest that the renin stimulatory effect of beta-adrenergic stimulation is not impaired by inhibition of PG synthesis, but baroreceptor stimulation of renin requires normal PG synthesis.