Evidence thatβ1-Adrenoceptor Activation Mediates Isoproterenol-Stimulated Renin Secretion in the Rat*

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Abstract
The goal of these experiments was to determine if isoproterenol-stimulated renin secretion in the rat is mediated by activation of .beta.1- and/or .beta.2-adrenoceptors. The rat renal cortical slice preparation was used. The renin secretory rate was a sigmoid function of the logarithm of the isoproterenol concentration; half-maximal and maximal stimulation occurred at .apprx. 0.01 and 0.1 .mu.M isoproterenol, respectively. Neither timolol (a nonselective .beta.-antagonist) nor atenolol (a .beta.1-selective antagonist) had a significant effect on basal secretory rate, but both shifted the isoproterenol dose-response curve to the right without changing its slope, suggesting competitive antagonism. Timolol was the more potent, but the response to maximally effective concentration of isoproterenol could be blocked by timolol (0.9 .mu.M), atenolol (110 .mu.M) or a combination of the 2 (0.45 .mu.M timolol plus 55 .mu.M atenolol). This latter finding is consistent with action of the 2 antagonists at one and the same site. If it is assumed that timolol antagonizes both .beta.1- and .beta.2-adrenoceptors and that atenolol antagonizes only .beta.1-adrenoceptors, it follows that isoproterenol-stimulated renin secretion in this preparation is mediated by activation of .beta.1-adrenoceptors.