Knape J T, van Zwieten P A
Division of Pharmacotherapy, Faculty of Medicine, University of Amsterdam, The Netherlands.
Arch Int Pharmacodyn Ther. 1988 Jan-Feb;291:142-52.
Vasopressin caused a potent vasoconstrictor effect in pithed rat preparations, without significantly altering heart rate. The vasopressor/constrictor response to vasopressin was not influenced by bilateral adrenalectomy, reserpine pretreatment or the prior administration of the alpha-adrenoceptor antagonists prazosin and yohimbine. The minor impairments of vasopressin-induced vasoconstriction by bilateral nephrectomy, captopril and the calcium entry blockers verapamil and nifedipine could all be attributed to the vasodilator potency of these various pretreatments. In conclusion, the potent vasoconstrictor response to vasopressin in the pithed rat occurs independently of the peripheral sympathetic nervous system and its associated adrenoceptors and of the renin-angiotensin-aldosterone systems. Moreover, vasopressin-induced vasoconstriction does not require the influx of extracellular calcium ions and is hence insensitive to calcium entry blockade. These findings for vasopressin reveal an important difference with respect to alpha 1/alpha 2-adrenoceptor agonists and angiotensin II, which are known to cause vasoconstriction largely dependent upon the influx of extracellular calcium ions.
血管加压素对去大脑大鼠标本有强大的血管收缩作用，且对心率无明显影响。血管加压素引起的升压/血管收缩反应不受双侧肾上腺切除术、利血平预处理或事先给予α-肾上腺素能受体拮抗剂哌唑嗪和育亨宾的影响。双侧肾切除术、卡托普利以及钙通道阻滞剂维拉帕米和硝苯地平对血管加压素诱导的血管收缩产生的轻微损害，均归因于这些不同预处理的血管舒张作用。总之，去大脑大鼠对血管加压素的强大血管收缩反应独立于外周交感神经系统及其相关的肾上腺素能受体以及肾素-血管紧张素-醛固酮系统。此外，血管加压素诱导的血管收缩不需要细胞外钙离子内流，因此对钙通道阻滞不敏感。血管加压素的这些发现揭示了与α1/α2-肾上腺素能受体激动剂和血管紧张素II的重要差异，已知后两者引起的血管收缩很大程度上依赖于细胞外钙离子内流。
