RELEASE OF β‐LIPOTROPIN‐ AND β‐ENDORPHIN‐LIKE MATERIAL INDUCED BY ANGIOTENSIN IN THE CONSCIOUS RAT

Abstract

1 The influence of the renin-angiotensin system on plasma β-endorphin-like immunoreactivity (β-EI) was investigated in the conscious rat by use of a radioimmunoassay for β-endorphin without prior extraction. 2 Intravenous infusion of angiotensin I, II or (des-1-Asp)angiotensin II (angiotensin III) caused a dose-dependent increase in plasma β-EI, angiotensin III infusion being less effective than angiotensin I or II. The plasma adrenocorticotrophin (ACTH) levels too were elevated by angiotensin II. The receptor antagonist, saralasin, prevented the angiotensin II-induced β-EI release as did dexamethasone pretreatment. 3 Both the release of β-EI and the pressor response to angiotensin I were abolished by the converting enzyme inhibitor, captopril (SQ 14225). In contrast, captopril did not affect the action of angiotensin II. 4 In view of the appreciable cross-reactivity of β-lipotropin (β-LPH) in our assay, plasma β-EI was analysed by Sephadex G-50 chromatography. In plasma extracts of angiotensin II-infused rats, immunoreactivity corresponding to human β-endorphin comprised about 49% of the total immunoreactivity, whereas 51% co-migrated with human β-LPH. 5 The increase in plasma levels of β-EI elicited by angiotensin II was diminished by about 35% in rats with a hereditary absolute lack of vasopressin (Brattleboro rats), when compared to normal rats. 6 These results suggest that the renin-angiotensin system can stimulate the secretion of β-LPH and β-endorphin with ACTH from rat anterior pituitary. One link in mediating the response appears to be vasopressin. The physiological function remains to be defined.