Glibenclamid - sensitive K + channels are responsible for angiotensin II hypersensitive contraction and atrial natriuretic factor refractoriness of glomeruli in low-sodium rats

Abstract

We investigated the role of ANF and potassium channels in dynamics of glomeruli isolated from low and normal-sodium rats. The ANG II - induced decrease glomerular size (36%) and (18%) in low and normal-sodium rats, respectively. ANF or cicletanine showed reversing effect on the ANG II - precontracted glomeruli from normal but not from low-sodium rats. The action of ANG II was abolished when ANF and cicletanine were added together. Glibenclamid completely abolished the inhibitory effect of cicletanine and ANF on ANG II - induced contraction of glomeruli from low-sodium rats. These results suggest that glibenclamid-sensitive potassium channels are responsible for ANG II hypersensitive contraction and ANF or cicletanine refractoriness of isolated glomeruli from low-sodium rats.