EVIDENCE FOR A SEPARATE ADENYLATE CYCLASE SYSTEM RESPONSIVE TO BETA-ADRENERGIC STIMULATION IN THE RENAL CORTEX OF THE RAT

Abstract

ABSTRACT Previous studies in other laboratories had indicated that some of the effects of parathyroid hormone on skeletal tissue and the renal tubule to influence ion metabolism can be produced by beta-adrenergic stimulation. Studies were carried out to determine whether the same adenylate cyclase system in rat renal cortex is activated by parathyroid hormone and isoproterenol. At maximal effective concentration of dose response, parathyroid hormone (2 × −5 m) increased adenylate cyclase activity by some 415 per cent, isoproterenol (10−6 m) increased activity by some 40 to 50 per cent, vasopressin (10−5 m) increased activity by some 96 per cent and porcine calcitonin (10−5 m) increased activity by some 92 per cent. Dl-propranolol (10−5 m), a beta-adrenergic receptor blocking agent, prevented the increase in enzyme activity produced by isoproterenol (10−6 m), did not diminish the increase in activity produced by parathyroid hormone (10−6 m) and did not influence basal adenylate cyclase activity by itself. The combined maximal concentrations of isoproterenol together with either parathyroid hormone, vasopressin or porcine calcitonin were additive. These results indicate that there is an adenylate cyclase system in rat renal cortex which can be activated by beta-adrenergic stimulation with isoproterenol, and is separate from the systems responsive to parathyroid hormone, vasopressin or calcitonin.