Abstract
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. First-order arterioles dilated from 72 +/- 3 microns to 93 +/- 4 microns in response to contraction of the cremaster muscle for 1 min (n = 7). After EDNO inhibition by topical application of 10 microM NW-nitro-L-arginine methyl ester (L-NAME), the resting diameter decreased to 66 +/- 3 microns and functional dilation was attenuated to 75 +/- 3 microns (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 microns vs. 89 +/- 3 microns, 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 micron, n = 7) equivalent to L-NAME. Norepinephrine treatment attenuated functional dilation to 77 +/- 3 microns which was to a level similar to L-NAME treatment (P > 0.05). Inhibition of prostaglandin synthesis by topical application of indomethacin (28 microM) resulted in no significant changes in the resting diameter but functional vasodilation was attenuated from 89 +/- 2 to 81 +/- 3 microns (n = 7, P < 0.05). 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.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call