Nitric oxide synthase inhibition increases vascular resistance in sodium and water loaded rats.

The aim of this study was to investigate whether nitric oxide might be involved in the adaptation of the cardiovascular system in sodium and water loaded organisms. The effects of a semi-chronic (4 day) inhibition of nitric oxide production were studied in normovolemic and per os sodium and water loaded rats. Nitric oxide synthase was inhibited by L-NAME (10 mg/kg in normovolemic and 14 mg/kg in sodium loaded rats) dissolved in the drinking solution. Blood pressure, cardiac output (Stewart-Hamilton's principle) and its regional fractions (Sapirstein's technique using 86Rb isotope as indicator), total peripheral resistance and regional vascular resistances were determined on the 5th day in sodium pentobarbital anaesthesia. The increase in blood pressure following L-NAME pretreatment in both groups was similar, but the elevation of total peripheral resistance was 106% in normovolemic and only 30% in sodium loaded animals. The cardiac output decreased by 44% in normovolemic and 14% in sodium loaded groups after nitric oxide synthase inhibition. The organ vascular resistances increased and organ blood flows decreased after L-NAME administration. These changes were less pronounced in sodium and water load, especially those in the skeletal muscle and intestine. Nitric oxide-induced changes in vascular resistance are more pronounced in normovolemia than in sodium load; sodium load might influence the nitric oxide production. The share of nitric oxide in the setting of vascular tone is different in the various organs.