The precise importance of prostaglandin (PG) in the β-adrenergic pathway to renin release is unresolved. Thus, we examined this question using renal cortical slices from Sprague-Dawley rats incubated in Krebs-Ringer bicarbonate mixture (KRB), KRB + isoproterenol (10-5 M, ISO), or a solution containing KRB + ISO + either propranolol (PRO, 10-5 M) or indomethacin (IN, 10-5 M). Media samples were assayed for renin activity, 6-keto-PGF(1α) (the stable metabolite of PGI2), and PGE2. ISO only increased renin release 1.96-fold; modest increments in 6-keto-PGF(1α) and PGE2 also occurred. The addition of PRO prevented these increases. In the next series of studies, ISO again increased renin, but the addition of IN failed to modify this increase in renin release. However, IN did prevent any increase in 6-keto-PGF(1α) or PGE2. Meclofenemate (10-5 M) provided results similar to those of IN. PGI2 was found to stimulate the release of renin in concentrations of 10-7 M. The combination of submaximal stimulatory concentrations of PGI2 (10-6 M, a 1.6-fold increment) and ISO (10-6 M, a 1.7-fold increment) produced a synergistic increase in renin release (2.84-fold). These results demonstrate that renal prostaglandins do not function as essential mediators of the β-adrenergic pathway to renin release. Rather, high concentrations of prostaglandins may increase the renin-releasing action of β-agonists, thereby modulating the release of renin.
|Original language||English (US)|
|Journal||American Journal of Physiology - Endocrinology and Metabolism|
|State||Published - 1984|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Physiology (medical)