Role of Endothelium-Derived Relaxing Factors in Arteriolar Dilation During Muscle Contraction Elicited by Electrical Field Stimulation

Objective: To determine the contribution of either endothelium-derived nitric oxide (EDNO) or prostaglandins in the functional vasodilation of first-order arterioles of the hamster cremaster muscle. Methods: First-order arterioles dilated from 72 ± 3 μm to 93 ± 4 μm in response to contraction of the cremaster muscle for 1 min (n = 7). After EDNO inhibition by topical application of 10 μM N^ω-nitro-l-arginine methyl ester (L-NAME), the resting diameter decreased to 66 ± 3 μm and functional dilation was attenuated to 75 ± 3 μm (P < 0.05). When the arteriolar diameter was returned to the control values by the addition of sodium nitroprusside, an NO donor, into the superfusion solution (n = 7), functional dilation was similar to that observed before EDNO inhibition (91 ± 3 μm vs. 89 ± 3 μm, P > 0.05). To evaluate whether the vasoconstrictor effect of L-NAME on functional dilation is same as other vasoconstrictors, norepinephrine was applied on the cremaster muscle to induce a vasoconstriction (72 ± 2 to 66 ± 1 μm, n = 7) equivalent to L-NAME. Results: Norepinephrine treatment attenuated functional dilation to 77 ± 3 μm which was to a level similar to L-NAME treatment (P > 0.05). Inhibition of prostaglandin synthesis by topical application of indomethacin (28 μM) resulted in no significant changes in the resting diameter but functional vasodilation was attenuated from 89 ± 2 to 81 ± 3 μm (n = 7, P < 0.05). Conclusions: These results suggest that EDNO is important for the resting tone of arterioles and that prostaglandins are important in modulating the functional dilation of the first-order arterioles in the hamster cremaster muscle.