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AN INVESTIGATION INTO THE TYPE OF β‐ADRENOCEPTOR MEDIATING SYMPATHETICALLY ACTIVATED RENIN RELEASE IN THE CAT
Author(s) -
JOHNS EDWARD J.
Publication year - 1981
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1981.tb16811.x
Subject(s) - isoprenaline , atenolol , endocrinology , medicine , plasma renin activity , stimulation , heart rate , propranolol , antagonist , chemistry , renin–angiotensin system , tachycardia , blood pressure , receptor
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 β‐adrenoceptor mediating this response. 2 In anaesthetized, unilaterally nephrectomized cats, a comparison was made of the ability of two selective β‐adrenoceptor antagonists to block the tachycardia and hypotension caused by isoprenaline (mediated respectively by β 1 ‐ and β 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 β 1 ‐adrenoceptor antagonist, atenolol (0.38 to 11.28μmol/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 β 2 ‐adrenoceptor antagonist, erythro‐DL‐(7‐methylindan‐4‐yloxy)‐3‐isopropylamino‐butan‐2‐ol (ICI 118, 551, 0.03 to 2.86μmol/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 β‐adrenoceptors mediating renin release resemble those in the heart more closely than those in peripheral blood vessels.