Aoi W, Henry D P, Weinberger M H
Circ Res. 1976 Feb;38(2).
Previous studies on renin release by an in vitro system of rat kidney slices, which is devoid of hemodynamic influences, have provided evidence that renin release is stimulated by a beta-adrenergic mechanism. We used this system to study effects of tyramine (an indirectly acting amine capable of displacing endogenous catecholmines from sympathetic nerve endings) on renin release. Tyramine (10(-3)M) in the presence of a monoamine oxidase inhibitor (pheniprazine, 10(-5)M) and a phosphodiesterase inhibitor (theophylline, 10(-3)M) significantly (P less than 0.01) stimulated renin release when values were compared to control observations for media containing only the inhibitors. Tyramine-induced stimulation of renin release was blocked by the beta-blocking agent, propranolol (2 X 10(-4) M), and the neural uptake blocking agent, cocaine (10(-5) M), but not by the alpha-antagonist, phentolamine (9 X 10(-4) M). These observations demonstrate a potential role for the sympathetic innervation of the juxtaglomerular apparatus on renin release.
先前利用无血流动力学影响的大鼠肾切片体外系统对肾素释放进行的研究表明,肾素释放受β-肾上腺素能机制刺激。我们利用该系统研究了酪胺(一种能够从交感神经末梢置换内源性儿茶酚胺的间接作用胺)对肾素释放的影响。当与仅含抑制剂的培养基的对照观察值相比时,在单胺氧化酶抑制剂(苯乙肼,10(-5)M)和磷酸二酯酶抑制剂(茶碱,10(-3)M)存在的情况下,酪胺(10(-3)M)显著(P<0.01)刺激了肾素释放。酪胺诱导的肾素释放刺激被β受体阻滞剂普萘洛尔(2×10(-4)M)和神经摄取阻滞剂可卡因(10(-5)M)阻断,但未被α拮抗剂酚妥拉明(9×10(-4)M)阻断。这些观察结果证明了肾小球旁器的交感神经支配在肾素释放中的潜在作用。