Selective inhibition by epinephrine of parathyroid hormone-stimulated adenylate cyclase in rat renal cortex
- 1 June 1982
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Renal Physiology
- Vol. 242 (6) , F721-F726
- https://doi.org/10.1152/ajprenal.1982.242.6.f721
Abstract
Parathyroid hormone- (PTH) stimulated adenylate cyclase activity in homogenates of rat renal cortex was inhibited by l-epinephrine. The specificity of the inhibition indicated that it was mediated by alpha 2-receptors. The inhibition of PTH-stimulated activity was greater than the inhibition of basal activity. The absolute decrease in adenylate cyclase activity produced by 10-4 M l-epinephrine was from 16.3 +/-0.6 (SE) to 11.2 +/- 0.6 pmol.min-1.mg-1 for activity stimulated by 10 microgram/ml PTH. Basal activity was decreased from 2.3 +/- 0.07 to 1.7 +/- 0.04. A similar inhibition of PTH-stimulated adenylate cyclase by l-epinephrine was demonstrated in preparations of renal cortical tubules. In contrast, the quantitative decrease in vasopressin-or calcitonin-stimulated activity by 10-4 M l-epinephrine was the same as the decrease in basal activity. These results demonstrate that PTH receptors that stimulated adenylate cyclase and alpha 2-adrenergic receptors that inhibit adenylate cyclase are present on the same cells in the renal tubules. Thus, a mechanism exists whereby alpha-adrenergic agonists can oppose the tubular actions of PTH via a direct inhibition of adenylate cyclase activity.This publication has 2 references indexed in Scilit:
- Regulation of adenylate cyclase of neuroblastoma x glioma hybrid cells by alpha-adrenergic receptors. I. Inhibition of adenylate cyclase mediated by alpha receptors.Journal of Biological Chemistry, 1979
- Mechanism of natriuresis and diuresis during elevated renal arterial pressureAmerican Journal of Physiology-Legacy Content, 1965