Hemodynamic and hormonal responses to 8-arginine-vasopressin in healthy man: effects of indomethacin.
Previous investigations suggest that in a normotensive organism the vasopressor effect of 8-arginine-vasopressin (AVP) is very effectively buffered by cardiovascular reflex mechanisms. Exogenous AVP administration shows only small, transient increases in blood pressure in spite of continued AVP-infusion and high plasma AVP concentrations. The present study aims to clarify the mechanism of the observed transient blood pressure elevations which are often referred to as "tachyphylaxis". Our results in healthy subjects show a two phase response to exogenous AVP: an initial phase which is characterized by cardiac reflex mechanisms and a second phase during which a normalisation of the elevated total peripheral resistance occurs. Inhibition of prostaglandin synthesis with indomethacin almost completely attenuates this vascular counterregulation to exogenous AVP, thus providing evidence that a prostaglandin mediated vasodilation in response to AVP may be the underlying mechanism for "vasopressin tachyphylaxis". The role of the renin-angiotensin-system and the importance of different regional hemodynamic effects of AVP are discussed.
D000328:Adult; D001127:Arginine Vasopressin / Q000494:pharmacology*; D002302:Cardiac Output / Q000187:drug effects; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology*; D008297:Male; D011453:Prostaglandins / Q000096:biosynthesis*; D012083:Renin / Q000097:blood; D013318:Stroke Volume / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects
D011453:Prostaglandins; D001127:Arginine Vasopressin; D012083:Renin; D007213:Indomethacin