Effects of nipradilol (K-351) on alpha-adrenoceptor mediated responses in various isolated tissues.
Effects of nipradilol (K-351) on alpha-adrenoceptor mediated responses in various isolated tissues.
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尼普地洛 (K-351) 对各种分离组织中 α-肾上腺素受体介导的反应的影响。
DOI：
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发表时间：
1985
影响因子：
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通讯作者：
K. Shigenobu
中科院分区：
文献类型：
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作者：
A. Ohira;Y. Wada;M. Fujii;M. Nakamura;Y. Kasuya;Y. Hamada;K. Shigenobu
尼普地洛竞争性拮抗去甲肾上腺素或去氧肾上腺素诱导的豚鼠胸主动脉收缩反应。尼普地洛的这些作用比酚妥拉明的作用大约低 6 倍。硝酸甘油对去甲肾上腺素引起的主动脉收缩表现出非竞争性拮抗作用。此外，尼普地洛竞争性抑制去甲肾上腺素诱导的大鼠输精管收缩，并剂量依赖性地降低去氧肾上腺素诱导的兔回肠抑制反应。尼普地洛的这些拮抗作用比酚妥拉明的拮抗作用弱 30 至 100 倍。硝酸甘油并没有明显影响大鼠输精管和兔回肠中α-肾上腺素受体介导的反应。可乐定对壁内刺激引起的大鼠输精管抽搐的抑制作用仅被尼普地洛轻微拮抗(pA2 = 5.4)。接触苯氧苯扎明后，尼普地洛和硝酸甘油对可乐定诱导的犬隐静脉收缩表现出非竞争性拮抗作用，而酚妥拉明则竞争性抑制可乐定反应。这些结果表明尼普地洛具有α1-肾上腺素受体阻断作用；它具有非常弱或几乎没有突触前α2阻断活性，但对突触后α2肾上腺素受体介导的收缩反应表现出非竞争性拮抗作用。
Nipradilol competitively antagonized norepinephrine- or phenylephrine-induced contractile responses of guinea-pig thoracic aorta. These actions of nipradilol were about 6 times less potent than those of phentolamine. Nitroglycerin showed a non-competitive antagonistic action on norepinephrine-induced contractions of aorta. Furthermore, nipradilol competitively inhibited norepinephrine-induced contractions of rat vas deferens and dose-dependently reduced the phenylephrine-induced inhibitory responses in rabbit ileum. These antagonistic actions of nipradilol were 30 to 100 times less potent than those of phentolamine. Nitroglycerin did not appreciably affect these alpha-adrenoceptor mediated responses in rat vas deferens and rabbit ileum. The inhibitory action of clonidine on the twitch contraction of rat vas deferens produced by intramural stimulation was only slightly antagonized by nipradilol (pA2 = 5.4). Nipradilol and nitroglycerin showed a non-competitive antagonistic action on clonidine-induced contractions of canine saphenous vein after the exposure to phenoxybenzamine, while phentolamine competitively inhibited the clonidine responses. These results suggest that nipradilol possesses an alpha 1-adrenoceptor blocking action; it possesses very weak or practically no presynaptic alpha 2-blocking activity but shows a non-competitive antagonistic action on postsynaptic alpha 2-adrenoceptor mediated contractile responses.