Winn M J, Gardiner S M, Bennett T
J Pharmacol Exp Ther. 1985 Nov;235(2):500-5.
The alpha adrenoceptor antagonists phenoxybenzamine and phentolamine are reported to have opposite effects on vasopressin release, the former inhibiting and the latter enhancing it. In this study we have assessed the functional involvement of vasopressin in the maintenance of blood pressure in conscious rats after administration of either phenoxybenzamine or phentolamine. In normal (Long-Evans) rats, phenoxybenzamine caused a small fall in arterial blood pressure, whereas phentolamine initially caused a profound hypotension which was followed by a fluctuating recovery back to normotensive levels. Similar effects were seen in rats deficient in hypothalamic vasopressin (Brattleboro strain). Administration of an antagonist of the cardiovascular actions of vasopressin [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid)-8-D-arginine vasopressin] in the presence of either alpha adrenoceptor antagonist alone was without effect in Long-Evans or Brattleboro rats, but, under these conditions, subsequent administration of captopril caused a profound and sustained hypotension in both strains. Administration of captopril in the presence of either alpha adrenoceptor antagonist alone caused a prompt fall in blood pressure which was sustained for the duration of the experiment in the Brattleboro rats. However, under these conditions, the blood pressure of the Long-Evans rats showed some recovery over the subsequent 45 min; this recovery was antagonized by [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid)-8-D-argine vasopressin]. It is concluded that after alpha adrenoceptor antagonism with either phenoxybenzamine or phentolamine, the renin-angiotensin system exerts a major pressor influence. However, after captopril administration in the presence of phenoxybenzamine or phentolamine, vasopressin contributes to the maintenance of arterial blood pressure in Long-Evans rats; the magnitude of this contribution is similar irrespective of the alpha adrenoceptor antagonist used.
据报道,α肾上腺素能受体拮抗剂酚苄明和酚妥拉明对血管加压素释放有相反的作用,前者抑制而后者增强其释放。在本研究中,我们评估了血管加压素在给予酚苄明或酚妥拉明后对清醒大鼠血压维持中的功能作用。在正常(长 Evans)大鼠中,酚苄明导致动脉血压小幅下降,而酚妥拉明最初引起严重低血压,随后血压波动恢复至正常血压水平。在下丘脑血管加压素缺乏的大鼠(布拉特洛维大鼠品系)中也观察到类似的效应。在单独使用任一α肾上腺素能受体拮抗剂的情况下,给予血管加压素心血管作用的拮抗剂[1-(β-巯基-β,β-环戊亚甲基丙酸)-8-D-精氨酸血管加压素]对长 Evans 大鼠或布拉特洛维大鼠均无影响,但在这些条件下,随后给予卡托普利会在两种品系大鼠中引起严重且持续的低血压。在单独使用任一α肾上腺素能受体拮抗剂的情况下给予卡托普利会导致血压迅速下降,在实验期间布拉特洛维大鼠的血压持续下降。然而,在这些条件下,长 Evans 大鼠的血压在随后的 45 分钟内出现了一些恢复;这种恢复被[1-(β-巯基-β,β-环戊亚甲基丙酸)-8-D-精氨酸血管加压素]拮抗。得出的结论是,在用酚苄明或酚妥拉明进行α肾上腺素能受体拮抗后,肾素-血管紧张素系统发挥主要的升压作用。然而,在酚苄明或酚妥拉明存在的情况下给予卡托普利后,血管加压素有助于维持长 Evans 大鼠的动脉血压;无论使用哪种α肾上腺素能受体拮抗剂,这种作用的程度相似。