title: Changes of blood pressure, plasma renin activity and plasma aldosterone concentration following the infusion of Sar1-Ile8-angiotensin II in hypertensive, fluid and electrolyte disorders.
abstract: 1-Sarcosine, 8-isoleucine angiotensin II (Sar1-Ile8-AII) was infused intravenously in 5 normal volunteers and 66 subjects with various hypertensive, fluid and electrolyte disorders. Changes of blood pressure (BP), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were studied. In normal subjects, Sar1-Ile-AII showed pressor (agonistic) activity, which was related to both dosage and sodium intake. Hyporeninaemic hypertensive subjects (pirmary aldosteronism) showed pressor responses to a smaller dose of this compound than the dose employed in normal subjects. Hyporeninaemic hypertensive subjects and normal volunteers after 3 days of high sodium intake showed significant elevations of BP and PAC and reduction of PRA. Changes of BP, PAC and PRA in normoreninaemic subjects including those with Bartter's syndrome, renal tubular acidosis or liver cirrhosis with ascites showed reduction of BP and PAC and elevation of PRA. The results indicate that the compound has both agonistic and antagonistic activities for blood pressure; which of these is obtained apparently depends upon endogenous angiotensin II levels, as well as the dosage employed. The results in subjects with high and low PRA suggest that the compound has antagonist and agonist actions at 3 sites of angiotensin II action, i.e. peripheral vascular bed, renin release mechanism from juxta-glomerular apparatus and the zona glomerulosa of the adrenals.
mesh_terms: D000141:Acidosis, Renal Tubular / Q000503:physiopathology; D000450:Aldosterone / Q000097:blood*; D000804:Angiotensin II / Q000031:analogs & derivatives* / Q000494:pharmacology; D001477:Bartter Syndrome / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects*; D003480:Cushing Syndrome / Q000503:physiopathology; D004487:Edema / Q000503:physiopathology; D006333:Heart Failure / Q000503:physiopathology; D006801:Humans; D006929:Hyperaldosteronism / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology*; D006974:Hypertension, Malignant / Q000503:physiopathology; D006977:Hypertension, Renal / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000503:physiopathology; D008103:Liver Cirrhosis / Q000503:physiopathology; D009404:Nephrotic Syndrome / Q000503:physiopathology; D010673:Pheochromocytoma / Q000503:physiopathology; D012083:Renin / Q000097:blood* / Q000502:physiology; D012964:Sodium / Q000502:physiology; D013997:Time Factors; D014883:Water-Electrolyte Imbalance / Q000503:physiopathology*
chemical_list: D000804:Angiotensin II; D000450:Aldosterone; D012964:Sodium; D012083:Renin