An intracerebral, physiological role for angiotensin: effects of central blockade.
Although exogenous angiotensin II (AII) exerts a multitude of effects on the central nervous system, there is little evidence supporting a physiological role for the endogenously produced peptide. Some investigators have tested the hypothesis that AII is physiologically active in the brain with intracerebral infusions of blockers of the renin-angiotensin system. If blocker infusions produce effects that are opposite to exogenous AII infusions, it is evidence supporting a physiological role for endogenously generated angiotensin. Previous work has demonstrated that intraventricular infusion of AII elicits thirst and stimulates antidiuretic hormone and ACTH release. Intracerebral administration of AII also suppresses aldosterone secretion. Experiments that employed the blockers saralasin, a competitive inhibitor of AII, and SQ 20881, a converting enzyme blocker, are presented; results suggest that endogenous AII is involved in the control of thirst and peripheral hormone levels. Infusion of the blockers in the ventricular system led to changes in peripheral hormone concentrations opposite to that observed following infusions of AII.
D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000450:Aldosterone / Q000378:metabolism; D000804:Angiotensin II / Q000494:pharmacology / Q000502:physiology*; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000502:physiology*; D004285:Dogs; D007276:Injections, Intraventricular; D012504:Saralasin / Q000494:pharmacology; D013722:Teprotide / Q000494:pharmacology; D013894:Thirst / Q000187:drug effects; D014667:Vasopressins / Q000378:metabolism
D014667:Vasopressins; D000804:Angiotensin II; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D013722:Teprotide; D012504:Saralasin