Sodium nitroprusside activates potassium channels in the vena cava in normotensive but not in hypertensive rats

Abstract

Despite the importance of the venous system in the regulation of blood pressure, there are few studies that evaluate venous function in health and disease, and the effects of drugs on venous function. Blood pressure depends directly on the peripheral resistance and cardiac output. Unlike the peripheral resistance, in which the contractile activity of the arteries is the key factor, cardiac output depends primarily on the venomotor tone. An increase in cardiac blood pressure can be caused by an increase in blood volume, structural changes in the walls of the veins, leading to a reduced compliance thereof, or an increase in the contractile activity of venous smooth muscle. This study examined the effect of sodium nitroprusside (SNP), a classical nitric oxide donor, on vascular relaxation in the vena cava from normotensive (2K) and renal hypertensive (2K-1C) rats. We studied the effect of this compound in vena cava rings from normotensive and renal hypertensive rats. We showed for the first time that the vascular relaxation induced by SNP is impaired in vena cavas from hypertensive rats because of an impaired functional activity of potassium channels. Another relevant finding of this study is that the sarcoplasmic reticulum Ca2+ ATPase is not involved in the venorelaxation induced by SNP.