Mori H, Chujo M, Tanaka E, Yamakawa A, Shinozaki Y, Mohamed M U, Nakazawa H
Department of Physiology, Tokai University School of Medicine, Kanagawa, Japan.
Am J Physiol. 1995 Mar;268(3 Pt 2):H1077-85. doi: 10.1152/ajpheart.1995.268.3.H1077.
We examined humoral and/or locally produced vasoactive factors involved in modulating sympathetic coronary vasoconstriction via the ATP-sensitive K (KATP) channel in 42 anesthetized dogs. Glibenclamide (30 micrograms.kg-1.min-1 ic or 0.6 mg.kg-1.min-1 left atrial injection) augmented coronary vascular resistance (CVR) at baseline and during cardiac sympathetic nerve stimulation (2-20 Hz), with a greater increase seen in the subepicardial region than in the subendocardial region both during beta-adrenergic receptor blockade and alpha- and beta-receptor blockade [P < 0.05 and P < 0.05 (n = 6 and 18 dogs), analysis of variance]. In contrast, pinacidil (10 micrograms.kg-1.min-1; n = 8 dogs) suppressed CVR. Glibenclamide enhanced CVR response to locally administered norepinephrine of 0.001-0.1 microgram.kg-1.min-1 (P < 0.05, analysis of covariance; n = 5 dogs) but did not enhance norepinephrine or neuropeptide Y overflow (n = 18 dogs). CVR was not modified by calcitonin gene-related peptide (CGRP) antagonist [CGRP-(8-37)], 8-phenyltheophylline, or N omega-nitro-L-arginine (n = 11 dogs). Thus sympathetic coronary vasoconstriction is modified by coronary vascular KATP channels with a transmural difference. However, CGRP, adenosine, and endothelial nitric oxide production are not involved in the modulation.
我们在42只麻醉犬中研究了通过ATP敏感性钾（KATP）通道调节交感神经介导的冠状动脉收缩的体液和/或局部产生的血管活性因子。格列本脲（30微克·千克⁻¹·分钟⁻¹静脉内注射或0.6毫克·千克⁻¹·分钟⁻¹左心房注射）在基线时以及心脏交感神经刺激（2 - 20赫兹）期间增加冠状动脉血管阻力（CVR），在β肾上腺素能受体阻断以及α和β受体阻断期间，心外膜下区域的增加幅度大于心内膜下区域[P < 0.05和P < 0.05（n = 6和18只犬），方差分析]。相比之下，吡那地尔（10微克·千克⁻¹·分钟⁻¹；n = 8只犬）可抑制CVR。格列本脲增强了对局部给予的0.001 - 0.1微克·千克⁻¹·分钟⁻¹去甲肾上腺素的CVR反应（P < 0.05，协方差分析；n = 5只犬），但未增强去甲肾上腺素或神经肽Y的溢出（n = 18只犬）。降钙素基因相关肽（CGRP）拮抗剂[CGRP - (8 - 37)]、8 - 苯基茶碱或Nω - 硝基 - L - 精氨酸对CVR无影响（n = 11只犬）。因此，交感神经介导的冠状动脉收缩通过冠状动脉血管KATP通道进行调节，且存在跨壁差异。然而，CGRP、腺苷和内皮一氧化氮的产生不参与这种调节。
