DIFFERENCES IN EDNO CONTRIBUTION TO ARTERIOLAR DIAMETERS AT REST AND DURING FUNCTIONAL DILATION IN STRIATED-MUSCLE

This study was designed to determine the physiological role of endothe lium-dependent nitric oxide (EDNO) in the control of arteriolar diamet er during rest and muscle stimulation. Diameters of first-, second-, a nd third-order arterioles in the superfused hamster cremaster muscle w ere measured before and throughout 1 min of field stimulation before a nd after inhibition of EDNO release. EDNO inhibition by intravenous N( omega)-nitro-L-arginine methyl ester (L-NAME) significantly attenuated the arteriolar vasodilation in response to 1 muM acetylcholine. First -order arterioles averaged 65 +/- 5 mum at rest and dilated to 86 +/- 6 mum during muscle stimulation (n = 9), second-order arterioles avera ged 45 +/- 6 mum and dilated to 72 +/- 3 mum during muscle stimulation (n = 6), with third-order arterioles averaging 29 2 mum, and dilating to 53 +/- 3 mum during muscle stimulation (n = 7). EDNO inhibition si gnificantly decreased both the resting diameter of first-order arterio les (57 +/- 4 mum) and functional dilation (68 +/- 3 mum; P < 0.05). E DNO inhibition had no effect on the resting diameter of second-order a rterioles (45 +/- 5 mum) yet significantly attenuated the functional d ilation (64 +/- 4 mum; P < 0.05). EDNO inhibition had no effect on eit her the resting diameter of third-order arterioles (30 +/- 2 mum) or t he functional dilation (49 +/- 2 mum). Thus EDNO inhibition decreases both the resting diameter and the functional dilation of first-order a rterioles, has no effect on the resting diameter of second-order arter ioles but impairs the functional dilation, and has no effect on either the resting diameter or functional dilation of third-order arterioles .