Barchowsky A, Data J L, Whorton A R
Prostaglandins. 1984 Jan;27(1):51-67. doi: 10.1016/0090-6980(84)90220-x.
Prostaglandins have been hypothesized to have several mechanistic functions in sympathetically mediated release of renin. The rabbit renal cortical slice system was chosen to examine the prostaglandin dependency of renin release directly stimulated by either a direct adenylate cyclase activator, forskolin, or a beta-agonist, isoproterenol. In this study, we demonstrate that with forskolin (1 X 10(-5) M) or isoproterenol (1 X 10(-6) M), renin release was elevated 2-3 fold above control, and that this increase was shown to accompany a substantial increase in the tissue levels of cAMP (19.5 fold and 3.5 fold respectively). We also demonstrate that the increase in renin release produced by these compounds was not inhibited by cyclooxygenase inhibitors, indomethacin (25 microM) or eicosatetraynoic acid (30 micrograms/ml), nor was it inhibited by the selective prostacyclin synthesis inhibitor, U-51605 (30 micrograms/ml). Each of these inhibitors was demonstrated to block the synthesis of prostaglandins in the cortical slices at the concentrations used. Thus we propose that prostaglandins do not play a role in the induction of renin release resulting from elevated cyclic nucleotide levels or beta-adrenergic stimulation.
前列腺素被推测在交感神经介导的肾素释放过程中具有多种机制功能。选用兔肾皮质切片系统来检测由直接腺苷酸环化酶激活剂福斯高林或β-激动剂异丙肾上腺素直接刺激引起的肾素释放对前列腺素的依赖性。在本研究中，我们证明，使用福斯高林（1×10⁻⁵ M）或异丙肾上腺素（1×10⁻⁶ M）时，肾素释放比对照组升高了2至3倍，并且这种增加伴随着组织中环磷酸腺苷（cAMP）水平的显著升高（分别为19.5倍和3.5倍）。我们还证明，这些化合物引起的肾素释放增加不受环氧合酶抑制剂吲哚美辛（25 μM）或二十碳四烯酸（30 μg/ml）的抑制，也不受选择性前列环素合成抑制剂U-51605（30 μg/ml）的抑制。已证明在所用浓度下，每种抑制剂均可阻断皮质切片中前列腺素的合成。因此，我们认为前列腺素在由环核苷酸水平升高或β-肾上腺素能刺激引起的肾素释放诱导过程中不起作用。
