NITRIC OXIDE MODULATION OF MICROVASCULAR RESPONSES IN THE DEOXYCORTICOSTERONE ACETATE-SALT HYPERTENSIVE RAT. 115

Abstract

Previous studies in our laboratory have demonstrated that arteriolar dilations mediated by stimulation of endogenously release nitric oxide release are depressed during an established stage of hypertension in spontaneously hypertensive rat (SHR). In the present study, we assessed the response of small arterioles in the cremaster muscle of DOCA-Salt hypertensive rats to stimulation of endogenous NO release and the effects of NO blockade or constrictor sensitivity to topically applied norepinephrine. Microvascular responses were assessed during an early stage (1 week after induction) and late stage (4 weeks after induction) of hypertension using intravital microscopy. Exposure to increasing concentrations of acetylcholine(10-10 - 10-5 M) produced a dose-dependent dilation of arterioles (16 ± 1 μm). This dilation was abolished in the presence of a 10-4 M bath concentration of Nw-nitro-L-arginine methyl ester (L-NAME), a specific antagonist of nitric oxide (NO) synthesis. L-NAME also produced reductions in resting arteriolar diameters that were attenuated in DOCA-Salt rats. These result suggest that basal and stimulated release of endogenous NO in the microcirculation of DOCA-Salt rats is attenuated.Funded by a grant from the American Heart Association.