Joshua I G
Department of Physiology and Biophysics, School of Medicine, University of Louisville, KY 40292.
Peptides. 1991 Jan-Feb;12(1):37-41. doi: 10.1016/0196-9781(91)90163-j.
The in vivo responsiveness of small arterioles and venules in the rat cremaster muscle to topical administration of neuropeptide Y was assessed using closed-circuit television microscopy. Male Sprague-Dawley rats were anesthetized with sodium pentobarbital (50 mg/kg) and the cremaster muscle was exposed to increasing bath concentrations of neuropeptide Y (10(-10)-10(-7) M). Neuropeptide Y produced dose-dependent constrictions in first (90 +/- 8 microns), second (50 +/- 6 microns) and third (21 +/- 4 microns) order arterioles. Arteriolar reactivity to the peptide was inversely related to vessel diameters. Venules were relatively unresponsive to neuropeptide Y. Exposure to the alpha-adrenergic receptor antagonist, phentolamine (10(-6) M), failed to modify the arteriolar constrictor responses to neuropeptide Y, while pretreatment with the sympathetic neuronal blocking agent, guanethidine (10(-5) M), produced a small, but significant, reduction in sensitivity. These data suggest that neuropeptide Y causes constriction of arterioles of skeletal muscle, primarily by acting directly on vascular smooth muscle to induce contraction, and not via release of endogenous norepinephrine.
采用闭路电视显微镜评估大鼠提睾肌中小动脉和小静脉对局部应用神经肽Y的体内反应性。雄性Sprague-Dawley大鼠用戊巴比妥钠（50mg/kg）麻醉，将提睾肌暴露于递增浴浓度的神经肽Y（10^(-10)-10^(-7)M）中。神经肽Y在一级（90±8微米）、二级（50±6微米）和三级（21±4微米）小动脉中产生剂量依赖性收缩。小动脉对该肽的反应性与血管直径呈负相关。小静脉对神经肽Y相对无反应。暴露于α-肾上腺素能受体拮抗剂酚妥拉明（10^(-6)M）未能改变小动脉对神经肽Y的收缩反应，而用交感神经阻滞剂胍乙啶（10^(-5)M）预处理则使敏感性有小幅但显著的降低。这些数据表明，神经肽Y引起骨骼肌小动脉收缩，主要是通过直接作用于血管平滑肌诱导收缩，而不是通过释放内源性去甲肾上腺素。
