Copper deficiency alters vasodilation in the rat cremaster muscle microcirculation.

摘要: The effects of copper deficiency on smooth muscle relaxation were studied in the cremaster microcirculation. Male Sprague-Dawley rats fed either a copper-adequate diet (CuA, 5 micrograms copper/g diet) or copper-deficient (CuD, no added copper) for 17-27 d before experimentation. In vivo television microscopy was used to quantify agonist-induced diameter changes third-order arterioles. Endothelium-dependent relaxation, which is hypothesized be mediated by nitric oxide, attenuated deficiency. Both receptor (acetylcholine, 10(-7) 10(-4) mol/L) and nonreceptor (calcium ionophore A23187, 10(-8) decreased. Nitric oxide-mediated dilation, endothelium-independent (10(-7) 10(-5) mol/L sodium nitroprusside), also Maximal responses as follows: acetylcholine, 136 +/- 16% CuA vs. 45 15% CuD; 104 21 11% nitroprusside, 125 12% 46 13% CuD. There difference microvascular dilation between groups treated with 10(-6) phosphodiesterase inhibitor papaverine (e.g., 109 CuD 133 21% mol/L). These results suggest that inhibits mechanism vascular without altering capacity relax. We decreases oxide radical availability disrupts oxide-guanylate cyclase interaction.