Article date: August 1982
By: U. BEUERS, G. HERTTING, W. KNEPEL in Volume 76, Issue 4, pages 579-585
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
DOI: 10.1111/j.1476-5381.1982.tb09257.x
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