Hypertensive mechanisms in coarctation of the aorta. Further studies of the renin-angiotensin system.
The mechanisms of hypertension in coarctation remain to be clearly defined. In other hypertensive states, abnormal plasma renin activity (PRA) has been unmasked by the depletion of extracellular volume and the use of angiotensin antagonists. In a group of patients with coarctation, preoperative and postoperative evaluations of the renin-angiotensin system have been performed. Before operation, a group of patients with coarctation and a group of normal control subjects both underwent salt restriction followed by diuresis. A standard angiotensin antagonist (saralasin) test was performed on the patients with coarctation, and they demonstrated excessive renin-angiotensin activity compared to the control subjects. Following operation, paradoxical hypertension developed in all of the patients. Repeat saralasin test in these patients again revealed excessive angiotensin activity in the same patients as preoperatively. It appears that the renin-angiotensin system plays a more active role in coarctation than previously believed.
D000293:Adolescent; D000804:Angiotensin II / Q000097:blood*; D001017:Aortic Coarctation / Q000097:blood* / Q000150:complications / Q000601:surgery; D002648:Child; D002675:Child, Preschool; D005665:Furosemide / Q000494:pharmacology; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000209:etiology; D012083:Renin / Q000097:blood*; D012504:Saralasin
D000804:Angiotensin II; D005665:Furosemide; D012083:Renin; D012504:Saralasin