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1- and β-adrenoceptors
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
1-adrenoceptor antagonist (bunazosin, 1 µmol/l), but was not altered by the addition of an
2-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
1-adrenoceptors. Accordingly, a dynamic balance may exist between β-adrenergic stimulation and
1-adrenergic depression of renin release.
Journal of Endocrinology (1992) 132, 133–140
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