title: Renin-angiotensin system and opioids during acute hemorrhage in conscious rabbits.
abstract: We measured changes in plasma renin activity (PRA) and used angiotensin-converting enzyme blockade with captopril to evaluate the role of the renin-angiotensin system during hemorrhage and after opioid receptor blockade in conscious rabbits. The increase in PRA after nonhypotensive hemorrhage was not statistically significant. PRA increased sixfold after a hypotensive hemorrhage to a mean arterial pressure less than 40 mmHg. This increase was statistically significant. Captopril altered the hemodynamic response to hemorrhage. The normal increase in vascular resistance early in hemorrhage was reduced by captopril pretreatment. After a critical blood loss, arterial pressure and heart rate decreased in both groups. The blood loss required to decrease mean arterial pressure to less than 40 mmHg was approximately 25% less in animals pretreated with captopril. The characteristic decrease in vascular resistance coincident with the onset of hypotension was still present after captopril pretreatment. Injection of naloxone or saline during acute hemorrhagic hypotension did not affect PRA. However, recovery of blood pressure after naloxone or saline was attenuated by converting-enzyme blockade. This attenuation was due primarily to a reduction in spontaneous recovery (i.e., recovery after the control saline injection) and not to a reduction in the response to naloxone. We tested whether this effect of captopril might be due to an interaction of ANG II and catecholamines. The plasma norepinephrine (NE) response to naloxone was statistically similar with and without captopril. In contrast, the response to exogenous NE after hypotensive hemorrhage was significantly reduced by captopril pretreatment. Captopril apparently did not alter baroreflex sensitivity but did reset the baroreflex to lower pressure levels during naloxone's pressor response.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Dalton Research Center, University of Missouri, Columbia 65211.
authors.forename: J C
authors.initials: JC
authors.lastname: Schadt
authors.forename: R R
authors.initials: RR
authors.lastname: Gaddis
mesh_terms: D000818:Animals; D002216:Captopril / Q000494:pharmacology; D004723:Endorphins / Q000502:physiology*; D006439:Hemodynamics / Q000187:drug effects; D006470:Hemorrhage / Q000097:blood / Q000503:physiopathology*; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D007703:Peptidyl-Dipeptidase A / Q000494:pharmacology; D011817:Rabbits; D011957:Receptors, Opioid / Q000187:drug effects / Q000502:physiology; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000502:physiology*; D012965:Sodium Chloride / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000502:physiology; D009435:Synaptic Transmission
chemical_list: D004723:Endorphins; D011957:Receptors, Opioid; D009270:Naloxone; D012965:Sodium Chloride; D002216:Captopril; D007703:Peptidyl-Dipeptidase A; D012083:Renin