[Participation of peptide mechanisms in physiological reactions of the cardiovascular system to hyperoxia].
Experimental study in 156 white rats with renovascular hypertension, posthemorrhagic hypotension and with normal blood pressure revealed that high--ressure oxygen (303.9 kPa--50 min) could activate angiotensin--converting enzyme, the latter taking part in inactivation of endogenous opioid peptides. Involvement of peptide--like links in hemodynamic responses to hyperoxia seems to be an important component of the mechanism of oxygen action upon the cardiovascular system.
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D000818:Animals; D002216:Captopril / Q000494:pharmacology; D002320:Cardiovascular Physiological Phenomena; D002319:Cardiovascular System / Q000187:drug effects*; D003000:Clonidine / Q000494:pharmacology; D004789:Enzyme Activation / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D006470:Hemorrhage / Q000503:physiopathology; D006931:Hyperbaric Oxygenation; D006978:Hypertension, Renovascular / Q000503:physiopathology; D007022:Hypotension / Q000503:physiopathology; D009020:Morphine / Q000494:pharmacology; D010100:Oxygen / Q000494:pharmacology*; D010455:Peptides / Q000502:physiology*; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D051381:Rats; D011957:Receptors, Opioid / Q000187:drug effects / Q000502:physiology
D010455:Peptides; D011957:Receptors, Opioid; D009020:Morphine; D002216:Captopril; D007703:Peptidyl-Dipeptidase A; D003000:Clonidine; D010100:Oxygen
Uchastie peptidnykh mekhanizmov v fiziologicheskikh reaktsiiakh serdechnko-sosudistoĭ sistemy na giperoksiiu.