An investigation into the type of beta-adrenoceptor mediating sympathetically activated renin release in the cat.

1 Stimulation of the renal nerves in the cat was previously shown to cause renin release which could be blocked by propranolol. An attempt was made in this study to determine the type of beta-adrenoceptor mediating this response.2 In anaesthetized, unilaterally nephrectomized cats, a comparison was made of the ability of two selective beta-adrenoceptor antagonists to block the tachycardia and hypotension caused by isoprenaline (mediated respectively by beta(1)- and beta(2)-adrenoceptors) and the release of renin caused by renal nerve stimulation.3 Isoprenaline (mean dose of 0.224 +/- 0.022 nmol/kg), increased heart rate by approximately 43 beats/min and decreased mean blood pressure by 47 mmHg. Stimulation of the distal cut ends of the renal nerves, at a rate sufficient to reduce renal blood flow by 30%, resulted in an approximately 150% increase in plasma renin activity.4 Administration of the selective beta(1)-adrenoceptor antagonist, atenolol (0.38 to 11.28 mumol/kg), caused a dose-related inhibition of nerve stimulated renin release and of isoprenaline-induced tachycardia, with no diminution of the vasodepressor response to isoprenaline; in contrast, the selective beta(2)-adrenoceptor antagonist, erythro-DL-(7-methylindan-4-yloxy)-3-isopropylamino-butan-2-ol (ICI 118, 551, 0.03 to 2.86 mumol/kg), caused a dose-related inhibition of the isoprenaline-induced vasodepression without altering the increase in plasma renin activity caused by renal nerve stimulation. Only at the highest dose of ICI 118, 551 was there a reduction of isoprenaline-induced tachycardia, by about 40%.5 The selective inhibition of neurally activated renin release by atenolol but not by ICI, 118, 551 is consistent with the suggestion that the beta-adrenoceptors mediating renin release resemble those in the heart more closely than those in peripheral blood vessels.