RENIN‐ANGIOTENSIN MEDIATION OF ADRENAL CATECHOLAMINE SECRETION INDUCED BY HYPOGLYCAEMIA IN THE CAT

MERLIN F. BUMPUS*, GIORA FEUERSTEIN, YEHUDA GUTMAN, MAHESH C. KHOSLA

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

The mechanism involved in catecholamine (CA) release from the cat adrenal gland in response to insulin hypoglycaemia was studied. In intact cats, hypoglycaemia induced an 11 fold increase in adrenomedullary CA secretion. Acute bilateral nephrectomy nearly abolished the increased CA release from the adrenal gland during hypoglycaemia. Infusion of Sar1‐Ileu8‐Angiotensin II (AII), a competitive AII antagonist, suppressed the adrenomedullary response to the insulin‐induced hypoglycaemia. After termination of the antagonist infusion, CA secretion from the adrenal medulla increased rapidly, reaching the same level as in insulin‐treated cats. Infusion of rabbit anti‐angiotensin I antibodies suppressed CA release from the adrenal gland of hypoglycaemic cats. This effect was more prolonged than that of Sar1‐Ileu8‐AII. These results indicate that CA release from the adrenal medulla of the cat in response to insulin‐induced hypoglycaemia, is mediated through the renal reninangiotensin system. Since hypoglycaemia causes sympathetic stimulation through a central mechanism, angiotensin may act through the central nervous system. 1980 British Pharmacological Society

Original languageEnglish
Pages (from-to)201-205
Number of pages5
JournalBritish Journal of Pharmacology
Volume69
Issue number2
DOIs
StatePublished - Jun 1980

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