Yamaguchi K, Karakida T, Koike M, Hama H
Department of Physiology, Niigata University School of Medicine, Japan.
Acta Endocrinol (Copenh). 1988 May;118(1):82-8. doi: 10.1530/acta.0.1180082.
To evaluate the roles for catecholamines in angiotensin II (ANG II)-induced vasopressin (AVP) release, we examined in conscious rats the effects of intraventricular (ivt) administrations of catecholamine antagonists on plasma AVP responses to ivt applications of its agonists and ANG II. Plasma AVP was determined by RIA using trunk blood collected after decapitation. Dopamine (0.15 mumol), phenylephrine (an alpha-adrenergic agonist, 0.15 mumol) or ANG II (48.2 pmol) augmented plasma AVP 90 sec after the injection, whereas after isoproterenol (a beta-adrenergic agonist, 0.15 mumol) plasma AVP was unaffected. The plasma AVP responses to both dopamine and ANG II were significantly (P less than 0.01) inhibited by haloperidol (a dopamine blocker, 0.15 mumol) given 10 min before administration of these agents. Pre-administration of phenoxybenzamine (an alpha antagonist, 0.15 mumol) which was confirmed to abolish the effect of phenylephrine, or propranolol (a beta antagonist, 0.15 mumol) did not block the effect of ANG II. Administration of haloperidol, phenoxybenzamine or propranolol alone was without effect on plasma AVP level. On the basis of these results, we concluded that ANG II-induced AVP secretion may be mediated and/or modulated by dopamine.
为评估儿茶酚胺在血管紧张素II(ANG II)诱导的血管加压素(AVP)释放中的作用,我们在清醒大鼠中研究了脑室内(ivt)给予儿茶酚胺拮抗剂对血浆AVP对ivt应用其激动剂和ANG II反应的影响。血浆AVP通过放射免疫分析法(RIA)测定,使用断头后采集的躯干血。注射后90秒,多巴胺(0.15 μmol)、去氧肾上腺素(一种α-肾上腺素能激动剂,0.15 μmol)或ANG II(48.2 pmol)可使血浆AVP升高,而异丙肾上腺素(一种β-肾上腺素能激动剂,0.15 μmol)对血浆AVP无影响。在给予这些药物前10分钟给予氟哌啶醇(一种多巴胺阻滞剂,0.15 μmol)可显著(P < 0.01)抑制血浆AVP对多巴胺和ANG II的反应。预先给予已证实可消除去氧肾上腺素作用的酚苄明(一种α拮抗剂,0.15 μmol)或普萘洛尔(一种β拮抗剂,0.15 μmol)并未阻断ANG II的作用。单独给予氟哌啶醇、酚苄明或普萘洛尔对血浆AVP水平无影响。基于这些结果,我们得出结论,ANG II诱导的AVP分泌可能由多巴胺介导和/或调节。