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C Kim, AM Roberts and IG Joshua
Department of Physiology and Biophysics, School of Medicine, University of Louisville, Kentucky, USA.
We previously found that capsaicin can dilate third-order arterioles in striated muscle by a mechanism that appears to involve release of endogenous calcitonin gene-related peptide (CGRP). Experiments were done to determine 1) whether capsaicin has similar effects on larger arterioles and venules and 2) whether relaxation involves endogenous CGRP and synthesis of endothelium-derived relaxing factor. In male Sprague-Dawley rats anesthetized with pentobarbital (50 mg/kg, i.p.), we examined responses of first- and second-order microvessels in the cremaster muscle using video microscopy. Addition of capsaicin (0.1 microgram/ml) to vessels constricted by norepinephrine (10(-7) M) dilated 1A's by 91% +/- 28%, 2A's by 113% +/- 18% 1V's by 11% +/- 6% and 2V's by 42% +/- 18%. Capsaicin in the presence of the specific CGRP receptor antagonist CGRP (8-37) caused an attenuated arteriolar dilation but had no significant venodilatory effect (1A's 29% +/- 18%, 2A's 55% +/- 14%, 1V's 7% +/- 3%, 2V's 16% +/- 3%). Pretreatment with N- nitro-L-arginine methyl ester (10(-4) M) did not prevent capsaicin- induced arteriolar dilation (A1's 118% +/- 11%; A2's 129 +/- 24%) but blocked capsaicin-induced venodilation (V1's constricted by 5% +/- 5%; V2's constricted by 2% +/- 6%). N-nitro-L-arginine methyl ester also blocked CGRP-induced dilation of both orders of venules, but not arterioles. These data suggest that capsaicin-induced dilation may involve synthesis of endothelium-derived relaxing factor in the venules but not in the arterioles.
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