Kubo T, Misu Y
Jpn J Pharmacol. 1981 Apr;31(2):221-6. doi: 10.1254/jjp.31.221.
Intraventricular administration of nicotine produced a biphasic effect, consisting of an initial rise than a slight fall in blood pressure in unanaesthetized rats. Spontaneously hypertensive rate (SHR) showed increased pressor responses, but these responses were within normal limits in renal hypertensive and DOCA-saline hypertensive rats. The blood pressure response to nicotine in SHR was abolished by intraventricular administration of hexamethonium, but not by atropine given via the same route. Central phentolamine and 6-hydroxydopamine did not affect the pressor response to nicotine. The pressor effect of nicotine in SHR was markedly diminished after removal of the adrenals and abolished after bilateral adrenalectomy plus peripheral 6-hydroxydopamine. These results indicate that the pressor response to intraventricular nicotine is increased in SHR. The pressor effect of nicotine may result from the activation of the central nicotinic receptor sites, which may cause the release of catecholamines both from the adrenal medulla and adrenergic nerve terminals.
在未麻醉的大鼠中，脑室内注射尼古丁产生双相效应，即血压先升高后略有下降。自发性高血压大鼠（SHR）的升压反应增强，但在肾性高血压大鼠和去氧皮质酮-生理盐水性高血压大鼠中，这些反应仍在正常范围内。脑室内注射六甲铵可消除SHR对尼古丁的血压反应，但经相同途径注射阿托品则不能。中枢酚妥拉明和6-羟基多巴胺不影响对尼古丁的升压反应。摘除肾上腺后，SHR对尼古丁的升压作用明显减弱，双侧肾上腺切除加外周6-羟基多巴胺后则完全消除。这些结果表明，SHR对脑室内尼古丁的升压反应增强。尼古丁的升压作用可能源于中枢烟碱受体位点的激活，这可能导致肾上腺髓质和肾上腺素能神经末梢释放儿茶酚胺。
