A biphasic effect of noradrenaline on renin release from rat juxtaglomerular cells in vitro is mediated by α1- and β-adrenoceptors

Abstract

ABSTRACT The direct effect of noradrenaline on renin release from juxtaglomerular (JG) cells in vitro were investigated in a dynamic superfusion system of dispersed rat renal cortical cells. At low concentrations (1–100 nmol/l), noradrenaline stimulated renin release in a dose-dependent manner, while at higher concentrations (0·1–1 mmol/l) it inhibited renin release. The stimulatory effect of 0·1 μmol noradrenaline/l was completely blocked by a β-adrenoceptor antagonist, propranolol (0·1 μmol/l). When applied at concentrations of 1 μmol/l or 10 μmol/l, noradrenaline had no consistent effect on renin release, although 10 μmol noradrenaline/l had an inhibitory effect in the presence of propranolol (0·1 μmol/l). The inhibitory effect of noradrenaline (0·1 mmol/l) was converted to a stimulatory effect by the addition of an α1-adrenoceptor antagonist (bunazosin, 1 μmol/l), but was not altered by the addition of an α2-adrenoceptor antagonist (yohimbine, 1 μmol/l). These results indicate that low concentrations of noradrenaline directly stimulate renin release from JG cells by the activation of β-adrenoceptors, while high concentrations of nor-adrenaline inhibit renin release by the activation of α1-adrenoceptors. Accordingly, a dynamic balance may exist between β-adrenergic stimulation and α1-adrenergic depression of renin release. Journal of Endocrinology (1992) 132, 133–140