Independence of β-adrenergic stimulation of renin release on renin synthesis

Rat renal cortical slices incubated in vitro released 7.0 ± 0.5% (mean ± SE, n = 30) of their total renin content into the incubation medium in 1 h. Isoproterenol (10^-6 M), a β-adrenergic agonist, caused a 75 ± 17% (n = 7) increase in renin release from the cortical slices. Treatment of the cortical slices with either cycloheximide or puromycin caused a significant 96.2 ± 0.34 (n = 8) or 98.5 ± 0.3% (n = 5), respectively, inhibition of protein synthesis. After protein synthesis and presumably renin synthesis was blocked with either cycloheximide or puromycin, isoproterenol was still able to increase significantly renin release from the cortical slices despite almost total blockade of protein synthesis. We conclude that a storage pool of renin may exist, since 1) only 7.0 ± 0.5% of the cortical slice renin content is released each hour, and 2) isoproterenol stimulation of renin release is not acutely dependent on renin synthesis. It is hypothesized that β-adrenergic stimulation of renin release is elicited from a storage pool of previously synthesized renin.