Effect Of Ace Inhibition In Renin-Angiotensin And Alpha(1)-Adrenergic Renal Vascular Renal Systems

The kidney is an important organ in the pathogenesis of hypertension and its complications, by the overactivation of intrarenal renin‐angiotensin system (RAS) and noradrenergic system leading to tissue injury. We evaluated captopril treatment at short and long term on Ang‐ II and phenylephrine‐induced renal vascular contraction and the participation of AT 1 receptor. Five weeks‐old WKY and SHR rats were treated with captopril at 30 mg/kg/day, in drinking water for 2 and 14 weeks and perfusion pressure on isolated kidney was measured. In WKY rats the systolic blood pressure was not affected by captopril and hypertension was absent in SHR. When kidney was stimulated with Ang II, surprisingly we observed an increase in vascular contraction and maximal effect in captopril‐treated rats, but no for the α 1 ‐adrenergic agonist phenylephrine. Losartan, AT 1 receptor antagonist blocked responses to Ang II in WKY but not in SHR. Our data show that treatment with captopril modifies the intrarenal vascular response via RAS and not by α 1 ‐adrenergic receptor pathway. It is possible that a different receptors population between strains might occur. [Supported by PAPIIT IN224408 and CONACYT 47481 grants; PC‐M is a doctoral fellow from CONACYT, 164454].