Among the pressor homeostatic mechanisms that appear after hemorrhage are renin-angiotensin response and aldosterone hypersecretion. Plasma renin activity (PRA) may decrease initially but increase always after a certain interval. Aldosterone secretion increases or decreases in a higher or lower degree. It is generally accepted that Ang II is one of the principal factors that stimulates aldosterone secretion, but from our material it resulted that after hemorrhage it evolves independently. This discrepancy is more evident if hemorrhage is followed by bilateral nephrectomy (BN), when PRA significantly decreases but aldosterone secretion increases. After a simple BN, PRA decreases significantly but aldosterone plasma concentration increases, a discrepancy that is more evident if BN are followed by hemorrhage. Thus, it appears that after hemorrhage, the aldosterone secretion is not stimulated by the renin-angiotensin system.
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