Effect of Hypertension Induced by Nitric Oxide Synthase Inhibition on Structure and Function of Resistance Arteries in the Rat

Publisher Website
Google Scholar
Abstract
To determine whether inhibition of generation of endothelium-derived relaxing factor or nitric oxide (NO) resulted in elevated blood pressure and its effect on resistance arteries, rats were offered NG-nitro-L-arginine methyl ester (L-NAME), a competitive inhibitor of NO synthase, in their drinking water. Blood pressure (BP) rose slightly from 100 ± 2 mmHg in controls to 130 ± 5 mmHg with 25 mg/Kg L-NAME per day and to 173 ± 9 mmHg with 100 mg/Kg per day for 2 1/2 to 4 weeks. Rats were studied after 1–2 weeks of hypertension (BP> 150 mmHg). The concentration of cyclic guanosine monophosphate, the intracellular second messenger of NO, was significantly depressed in aorta and in the mesenteric vascular bed in L-NAME-treated rats. Mesenteric resistance arteries studied on a wire-myograph exhibited similar external and lumen diameters, whereas media width and media/lumen ratio were greater (p8 vasopressin was similar. In conclusion, administration of an NO synthase inhibitor produces hypertension, with exaggerated media/lumen ratio in resistance arteries and enhancement of response to norepinephrine, which together with decreased NO generation may contribute to elevation of blood pressure.