Intra-cerebroventricular captopril reduces plasma ACTH and vasopressin responses to hemorrhagic stress.
The role of the brain renin-angiotensin system in mediating the peripheral hormone response to acute hemorrhagic stress (15 ml/kg over 10 min) was studied in 6 sheep during an intracerebroventricular infusion (2.8 micrograms/min) of the angiotensin-converting enzyme inhibitor, captopril. When compared with control experiments the plasma ACTH and vasopressin (AVP) response to hemorrhage was markedly reduced and delayed during icv captopril, which did not affect the response of plasma angiotensin II (AII). These results suggest that the normal and rapid response in ACTH and AVP secretion accompanying hemorrhagic stress is dependent on increased brain production of AII.
D000324:Adrenocorticotropic Hormone / Q000097:blood*; D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001127:Arginine Vasopressin / Q000097:blood*; D002216:Captopril / Q000008:administration & dosage / Q000494:pharmacology*; D002552:Cerebral Ventricles; D004837:Epinephrine / Q000097:blood; D005260:Female; D006339:Heart Rate; D006470:Hemorrhage / Q000097:blood*; D009638:Norepinephrine / Q000097:blood; D012756:Sheep; D013312:Stress, Physiological / Q000097:blood*
D000804:Angiotensin II; D001127:Arginine Vasopressin; D000324:Adrenocorticotropic Hormone; D002216:Captopril; D009638:Norepinephrine; D004837:Epinephrine