Role of angiotensin in lethal cerebral hypoperfusion during treatment of acute hypertension.
A 23-year-old man developed lethal cerebral hypoperfusion associated with angiographically demonstrable cerebral arterial spasm while being treated for acute angiotensinogenic hypertension due to a traumatic coarctation of the aorta. This complication occurred even though the treatment maintained his blood pressure at normotensive to mildly hypertensive levels, without producing more than rare and fleeting periods of hypotension. To explain this enigmatic development, we propose that the high concentration of angiotensin II in the blood constricted the cerebral arteries and thus prevented adequate cerebral autoregulation when his blood pressure was lowered by drug therapy.
D000208:Acute Disease; D000328:Adult; D000804:Angiotensin II / Q000097:blood / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects; D002533:Cerebral Angiography; D002536:Cerebral Arteries / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D002546:Ischemic Attack, Transient / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology; D008297:Male; D009599:Nitroprusside / Q000627:therapeutic use; D010477:Perfusion; D014661:Vasoconstriction
D000804:Angiotensin II; D009599:Nitroprusside