Flow-induced vasodilation in hamster cremasteric arterioles was investigated with special reference to the roles of nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). Arterioles (∼60 µm resting diameter) were cannulated, and suffused with MOPS solution at 37°C (mean intraluminal pressure: 80 cm H2O). Step increases in the perfusate flow elicited a dose-dependent vasodilation, which was almost proportional to the increases in calculated wall shear stress (WSS). Nω-nitro L-arginine methyl ester (L-NAME, 100 µM) reduced the flow-induced vasodilation by ∼50%, whereas indomethacin (10 µM) produced no significant effect. In the presence of L-NAME, the residual vasodilation was eliminated by treatment with the cytochrome P-450 monooxygenase inhibitor 17-octadecynoic acid (17-ODYA, 50 µM), sulfaphenazol (10 µM), tetraethylammonium (TEA, 3 mM; a nonselective Ca2+-activated K+ channel inhibitor), or charybdotoxin (ChTX, 0.1 µM; intermediate or large conductance Ca2+-activated K+ channel inhibitor). In the absence of L-NAME, the dilation was also reduced by ∼50% by treatment with 17-ODYA, TEA, or ChTX. The residual vasodilation was eliminated by additional treatment with L-NAME. The inhibitor of ATP-sensitive K+ channels (KATP), glibenclamide, also caused a significant, but partial, reduction of the flow-induced vasodilation. The residual vasodilation was completely reduced by additional treatment with 17-ODYA, but not L-NAME. These findings suggest that in hamster cremaster, higher flow rate produces NO, KATP, and EDHF vasodilation of the arterioles under physiological conditions.

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