Bergmann C, Schoeffter P, Stoclet J C, Gairard A
Laboratoire de pharmacodynamie, INSERM U243, Faculté de pharmacie, Université Louis Pasteur, Strasbourg, France.
Can J Physiol Pharmacol. 1987 Nov;65(11):2349-53. doi: 10.1139/y87-372.
Experiments were designed to further investigate the vasoactive mechanisms of parathyroid hormone (PTH) on vascular smooth muscle cells. Time courses of the cAMP responses to the fragment (1-34) of bovine PTH (bPTH(1-34)) on cAMP levels have been studied in rat isolated aorta and in aortic myocytes in primary culture. In both aorta and myocytes bPTH (1-34) induced an increase in cAMP levels that was maximal and reached, respectively, 1.6- and 1.9-fold the basal level after 2 min of contact with bPTH (1-34). The effect of bPTH (1-34) on aortic cAMP content was concentration dependent in the range of 30-300 nM. (Nle8,18, Tyr34)-bPTH (3-34)amide, an antagonist of bPTH (1-34) with a stimulant effect on renal and vascular adenylate cyclase activity, inhibited the cAMP-increasing effect of bPTH (1-34). These results are in favour of a role for cAMP in the vasodilating effect of PTH.
设计实验以进一步研究甲状旁腺激素(PTH)对血管平滑肌细胞的血管活性机制。在大鼠离体主动脉和原代培养的主动脉肌细胞中,研究了牛PTH(bPTH(1-34))片段(1-34)对cAMP水平的cAMP反应时间进程。在主动脉和肌细胞中,bPTH(1-34)均诱导cAMP水平升高,与bPTH(1-34)接触2分钟后,cAMP水平分别达到最大值,分别为基础水平的1.6倍和1.9倍。bPTH(1-34)对主动脉cAMP含量的影响在30-300 nM范围内呈浓度依赖性。(Nle8,18, Tyr34)-bPTH(3-34)酰胺是bPTH(1-34)的拮抗剂,对肾脏和血管腺苷酸环化酶活性有刺激作用,它抑制了bPTH(1-34)增加cAMP的作用。这些结果支持cAMP在PTH血管舒张作用中的作用。