Helwig J J, Schleiffer R, Judes C, Gairard A
Life Sci. 1984 Dec 24;35(26):2649-57. doi: 10.1016/0024-3205(84)90034-1.
The effect of the synthetic amino-terminal fragment of bovine parathyroid hormone, bPTH-(1-34), on the adenylate cyclase of microvessels and glomeruli isolated from rabbit kidney cortex was studied in the presence and absence of guanosine triphosphate (GTP). bPTH-(1-34) stimulated the vascular and glomerular adenylate cyclase in a dose-dependent manner with apparent ED50 values of 11.5 nM and 64 nM respectively, in the absence of GTP. 10(-4)M GTP greatly amplified the vascular response to bPTH-(1-34) while, in the glomeruli, both GTP and bPTH-(1-34) had only additive effects. In the presence of GTP, vascular and glomerular apparent ED50 were 190 nM and 64 nM respectively. [Nle8, Nle18, Tyr34] -bPTH-(3-34) amide, described as a PTH antagonist, inhibited the action of bPTH-(1-34) in the microvessels and to a lesser extent in the glomeruli. PTH is therefore a potent stimulator of adenylate cyclase in rabbit renal microvessels and glomeruli, and may play a role in the regulation of renal blood flow and glomerulo-tubular feedback control.
在存在和不存在三磷酸鸟苷（GTP）的情况下，研究了牛甲状旁腺激素的合成氨基末端片段bPTH-(1-34)对从兔肾皮质分离的微血管和肾小球腺苷酸环化酶的影响。在不存在GTP的情况下，bPTH-(1-34)以剂量依赖性方式刺激血管和肾小球腺苷酸环化酶，表观ED50值分别为11.5 nM和64 nM。10(-4)M GTP极大地增强了血管对bPTH-(1-34)的反应，而在肾小球中，GTP和bPTH-(1-34)仅具有相加作用。在存在GTP的情况下，血管和肾小球的表观ED50分别为190 nM和64 nM。被描述为甲状旁腺激素拮抗剂的[Nle8, Nle18, Tyr34] -bPTH-(3-34)酰胺抑制了bPTH-(1-34)在微血管中的作用，在肾小球中的抑制作用较小。因此，甲状旁腺激素是兔肾微血管和肾小球腺苷酸环化酶的有效刺激剂，可能在肾血流调节和肾小球-肾小管反馈控制中起作用。
