Aikawa J, Moroi M, Namiki A, Yamaguchi T, Machii K, Koike K, Takayanagi I
Third Department of Internal Medicine, Ohashi Hospital, Toho University School of Medicine, Tokyo, Japan.
Heart Vessels. 1993;8(4):176-80. doi: 10.1007/BF01744739.
We investigated the mechanism of vascular relaxation produced by denopamine (deno), an oral positive inotropic agent that has selective beta 1-adrenergic action. Deno concentration-dependently (0.1 microM-30 microM) relaxed ring segments of canine femoral, mesenteric, and renal arteries which were partially precontracted with 1 micron phenylephrine or norepinephrine, but did not relax those precontracted with 5 microM prostaglandin F2 alpha or 40 mM K+. The relaxation was not significantly inhibited by pretreatment with 10 microM propranolol or metoprolol. Deno produced a parallel rightward shift in concentration-response curves to phenylephrine in femoral and renal arteries. The Schild plot yielded linear regressions of slopes of 1.301 +/- 0.106 and 0.823 +/- 0.122, respectively, which were not significantly different from unity. The pA2 values of Deno against phenylephrine in femoral and renal arteries were 5.41 +/- 0.03 and 5.76 +/- 0.06, respectively. On the other hand, Deno concentration-dependently (10 nM-10 microM) relaxed ring segments of canine coronary arteries which were partially precontracted with 5 microM prostaglandin F2 alpha. The relaxation was significantly inhibited by pretreatment with 10 microM metoprolol. In conclusion, vascular smooth muscle relaxation by Deno was mediated through beta 1-adrenergic action in canine coronary arteries and through the blocking effect of alpha-adrenoceptors in canine femoral, mesenteric, and renal arteries.
我们研究了口服正性肌力药物多巴胺（deno）产生血管舒张的机制，该药物具有选择性β1 - 肾上腺素能作用。Deno浓度依赖性地（0.1微摩尔/升 - 30微摩尔/升）使犬股动脉、肠系膜动脉和肾动脉的环段舒张，这些动脉环段已用1微摩尔/升去氧肾上腺素或去甲肾上腺素部分预收缩，但对用5微摩尔/升前列腺素F2α或40毫摩尔/升钾预收缩的动脉环段无舒张作用。用10微摩尔/升普萘洛尔或美托洛尔预处理并未显著抑制这种舒张作用。Deno使股动脉和肾动脉对去氧肾上腺素的浓度 - 反应曲线平行右移。Schild图分别得出斜率为1.301±0.106和0.823±0.122的线性回归，与1无显著差异。Deno在股动脉和肾动脉中对抗去氧肾上腺素的pA2值分别为5.41±0.03和5.76±0.06。另一方面，Deno浓度依赖性地（10纳摩尔/升 - 10微摩尔/升）使犬冠状动脉环段舒张，这些环段已用5微摩尔/升前列腺素F2α部分预收缩。用10微摩尔/升美托洛尔预处理可显著抑制这种舒张作用。总之，表示在犬冠状动脉中，Deno引起的血管平滑肌舒张是通过β1 - 肾上腺素能作用介导的，而在犬股动脉、肠系膜动脉和肾动脉中是通过α - 肾上腺素能受体的阻断作用介导的。
