title: Endogenous opioid mechanisms in hypothalamic blood flow autoregulation during haemorrhagic hypotension and angiotensin-induced acute hypertension in cats.
abstract: The influence of naloxone-induced general opiate receptor blockade on hypothalamic blood flow autoregulation was investigated in anaesthetized, artificially ventilated, temperature controlled cats. In order to study the changes of the hypothalamic blood flow (H2-gas clearance technique) at the lower limit of autoregulation systemic arterial pressure was reduced in a stepwise manner to 100, 80, 60 and 40 mmHg, by haemorrhage. Autoregulatory mechanisms of the hypothalamic vessels remained effective and hypothalamic blood flow showed no significant reduction until the arterial pressure was reduced to 60 mmHg in the vehicle-treated control cats. General opiate receptor blockade by 1 mg kg-1 mL-1 i.v. injected naloxone resulted in a significant reduction of the autoregulatory capacity of the hypothalamic vessels: the blood flow followed passively the arterial pressure fall already from 100 mmHg mean arterial pressure. The effect of opiate receptor blockade on the upper limit of the autoregulation was studied during acute arterial hypertension, induced by angiotensin-II infusion (25 micrograms 0.1 mL-1 min-1 i.v.). Hypothalamic blood flow remained remarkably steady following angiotensin-II infusion in the saline-treated control animals. Naloxone pretreatment (1 mg kg-1 mL-1 i.v.), however, induced a significant downward shift of the upper limit of the autoregulation, and hypothalamic blood flow started to increase in the 125-145 mmHg arterial pressure range. The narrowing of the autoregulatory range following general opiate receptor blockade suggests an important role of endogenous opioid peptides in hypothalamic blood flow autoregulatory mechanisms both in hypotensive and in hypertensive conditions.
authors: Experimental Research Department-2nd Institute of Physiology, Semmelweis University of Medicine, Budapest, Hungary.
authors: K
authors: K
authors: Komjáti
authors: M
authors: M
authors: Velkei-Harvich
authors: J
authors: J
authors: Tóth
authors: G
authors: G
authors: Dallos
authors: I
authors: I
authors: Nyáry
authors: P
authors: P
authors: Sándor
mesh_terms: D000804:Angiotensin II / Q000009:adverse effects; D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D002415:Cats; D002496:Central Venous Pressure; D002560:Cerebrovascular Circulation / Q000502:physiology; D005260:Female; D006470:Hemorrhage / Q000150:complications / Q000503:physiopathology; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D007022:Hypotension / Q000150:complications / Q000503:physiopathology*; D007031:Hypothalamus / Q000098:blood supply*; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D011957:Receptors, Opioid / Q000502:physiology*
chemical_list: D009292:Narcotic Antagonists; D011957:Receptors, Opioid; D000804:Angiotensin II; D002245:Carbon Dioxide; D009270:Naloxone