Interaction of atriopeptin III and vasopressin on calcium kinetics and contraction of aortic smooth muscle cells.
Interaction of atriopeptin III and vasopressin on calcium kinetics and contraction of aortic smooth muscle cells.
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心房肽 III 和加压素对钙动力学和主动脉平滑肌细胞收缩的相互作用。
DOI：
10.1172/jci113745
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Schrier,RW
中科院分区：
文献类型：
--
作者：
Meyer-Lehnert,H;Caramelo,C;Tsai,P;Schrier,RW
本文研究了心房肽Ⅲ（AP Ⅲ）对血管加压素（AVP）引起的血管平滑肌细胞（VSMC）Ca ~（2+）动员和细胞形态改变的舒张作用的细胞机制。APIII（10（-8）M）可抑制10（-8）M AVP诱导的细胞内游离Ca ~（2+），[Ca ~（2+）]i的升高（234.0 +/- 14.8 vs. 310.0 +/- 28.4 nM，P <0.01）。在45 Ca ~（2+）外排实验中也得到了类似的结果。然而，APIII（10（-7）M）没有改变AVP诱导的三磷酸肌醇（IP 3）的产生，尽管肌醇-1-磷酸的水平显著降低。APIII阻断或减弱AVP诱导的Ca 2+动员的作用与抑制AVP刺激的细胞形状变化有关。然而，心房钠尿因子（ANF）对细胞形状的影响，发生在较低的ANF浓度比对Ca 2+动员的影响。APIII刺激VSMC产生环磷酸鸟苷（cGMP）。APIII对AVP刺激的Ca 2+动员的作用部分被稳定的核苷酸8-溴cGMP模拟，而不受可溶性鸟苷酸环化酶抑制剂亚甲蓝（10（-4）M）的影响。这些结果表明，APIII发挥其血管舒张作用，在一定程度上，通过干扰血管加压素刺激的血管平滑肌细胞中的Ca 2+动员，也许通过刺激颗粒鸟苷酸环化酶和cGMP。然而，ANF对收缩机制的影响，在一个网站独立的Ca 2+释放也建议本研究结果。
The cellular mechanism of the vasodilatory action of atriopeptin III (APIII) on vasopressin (AVP)-induced Ca2+ mobilization and cell shape change in cultured vascular smooth muscle cells (VSMC) was studied. APIII (10(-8) M) attenuated the increase of intracellular free Ca2+, [Ca2+]i, induced by 10(-8) M AVP (234.0 +/- 14.8 vs. 310.0 +/- 28.4 nM, P less than 0.01). Similar results were obtained in 45Ca2+ efflux experiments. APIII (10(-7) M), however, did not alter AVP-induced inositol trisphosphate (IP3) production, although the levels of inositol-1-phosphate were significantly reduced. The effect of APIII to block or attenuate AVP-induced Ca2+ mobilization was associated with an inhibition of AVP-stimulated cell shape change. The effect of atrial natriuretic factor (ANF) on cell shape, however, occurred at lower ANF concentrations than the effect on the Ca2+ mobilization. APIII stimulated production of cyclic guanosine monophosphate (cGMP) in VSMC. The effect of APIII on AVP-stimulated Ca2+ mobilization was partially mimicked by the stable nucleotide 8-bromo cGMP and was not affected by the soluble guanylate cyclase inhibitor, methylene blue (10(-4) M). These results suggest that APIII exerts its vasodilatory effect, in part, by interference with vasopressor-stimulated Ca2+ mobilization in vascular smooth muscle cells, perhaps by stimulating particulate guanylate cyclase and cGMP. However, an effect of ANF on the contractile mechanism at a site independent of Ca2+ release is also suggested by the present results.