Na+-K+ cotransport and hypertension. Effect of piretanide and hydrochlorothiazide on red blood cell sodium concentration in acutely salt-loaded hypertensive and normotensive rats.

Abstract

Na+-K+ cotransport has been presumed to be a genetic marker or aetiological factor in essential hypertension in numerous studies. In spite of extended in vitro research, the role of this transport system in hypertension could not be proved. In the present study the action of the cotransport inhibitor piretanide and the non-loop diuretic hydrochlorothiazide (HCT) on red blood cell (RBC) sodium concentration was examined under in vivo conditions in spontaneously hypertensive rats (SHR) and normotensive Sprague Dawley rats (NSDR) during acute salt-loading. Before drug administration salt-loading resulted in an increase of RBC sodium concentration, the percentage of which was not different in SHR and NSDR. However, after administration of piretanide in oral doses of 8-32 mg/kg body weight, the percent increase in RBC sodium was lower in SHR than in NSDR. This effect which was found to be dose-dependent was not brought about by HCT. The data might be due to a piretanide inhibition of sodium-induced inward RBC Na+-K+ cotransport more pronounced in SHR than in NSDR.