Petit P, Barberis C, Jard S
Centre C.N.R.S.-INSERM de Pharmacologie-Endocrinologie, Montpellier, France.
Brain Res. 1988 Feb 9;440(2):299-304. doi: 10.1016/0006-8993(88)90999-7.
Previous experiments gave biochemical and electrophysiological evidence for the presence of functional V1-vasopressin receptors coupled to inositol lipid metabolism, but not to cyclic AMP accumulation in the rat superior cervical ganglion. This work was designed to investigate whether there was an action of vasopressin on the noradrenaline-induced cyclic AMP accumulation through the activation of phospholipase C. Our results clearly demonstrate that arginine-vasopressin potentiates cyclic AMP accumulation induced by noradrenaline or isoproterenol in a concentration-dependent manner. The potentiation was unaffected by phentolamine, but was suppressed by the V1-type vasopressin receptor antagonists. Moreover, the phorbol ester 4 beta-phorbol-12-myristate-13-acetate (TPA) did not affect this potentiation which seemed to be Ca2+-dependent. The results suggest that vasopressin may modulate the activity of autonomous functions in the sympathetic ganglia.
先前的实验提供了生化和电生理证据,表明大鼠颈上神经节中存在与肌醇脂质代谢偶联的功能性V1-血管加压素受体,但与环磷酸腺苷(cAMP)积累无关。这项研究旨在调查血管加压素是否通过激活磷脂酶C对去甲肾上腺素诱导的cAMP积累产生作用。我们的结果清楚地表明,精氨酸血管加压素以浓度依赖的方式增强去甲肾上腺素或异丙肾上腺素诱导的cAMP积累。这种增强不受酚妥拉明的影响,但被V1型血管加压素受体拮抗剂抑制。此外,佛波酯4β-佛波醇-12-肉豆蔻酸酯-13-乙酸酯(TPA)不影响这种似乎依赖Ca2+的增强作用。结果表明,血管加压素可能调节交感神经节中自主功能的活动。