Morris B J, Reid I A, Ganong W F
Eur J Pharmacol. 1979 Oct 26;59(1-2):37-45. doi: 10.1016/0014-2999(79)90022-0.
A variety of alpha-adrenergic agonists encompassing a broad range of concentrations were used to investigate the existence and nature of a putative alpha-adrenergic mechanism inhibitory to renin release, which may operate at the level of the juxtaglomerular apparatus. For this purpose rat renal cortical tissue incubated in vitro was used. Concentrations of noradrenaline, adrenaline and methoxamine of 10(-6), 10(-5), 10(-4) and 10(-3) M caused significant dose-related inhibition of renin release. The inhibition of release by these doses was reversed completely by 10(-4) M phentolamine. In contrast, phenylephrine, oxymetazoline and clonidine did not inhibit renin release. The results support the concept of an alpha-adrenergic mechanism inhibitory to renin release and show that high concentrations of alpha-adrenergic agonist are required for its operation in vitro. The manner in which this inhibitory mechanism affects renin release under physiological circumstances remains to be demonstrated.
使用了一系列浓度范围广泛的α-肾上腺素能激动剂,以研究可能存在的抑制肾素释放的α-肾上腺素能机制的存在及性质,该机制可能在肾小球旁器水平发挥作用。为此,采用了体外培养的大鼠肾皮质组织。去甲肾上腺素、肾上腺素和甲氧明浓度为10(-6)、10(-5)、10(-4)和10(-3)M时,可引起肾素释放显著的剂量相关抑制。这些剂量引起的释放抑制可被10(-4)M酚妥拉明完全逆转。相比之下,去氧肾上腺素、羟甲唑啉和可乐定并不抑制肾素释放。结果支持存在抑制肾素释放的α-肾上腺素能机制这一概念,并表明在体外发挥作用需要高浓度的α-肾上腺素能激动剂。这种抑制机制在生理情况下影响肾素释放的方式仍有待证明。