Synthetic atrial peptide inhibits intracellular calcium release in smooth muscle.-猫眼课题宝

合成心房肽抑制平滑肌细胞内钙的释放。

DOI：

发表时间：

1986

期刊：

American Journal of Physiology

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通讯作者：

中科院分区：

文献类型：

作者：

K. Meisheri;C. Taylor;H. Saneii

本文观察了人工合成的心房肽(Atriopeptin II，AP II)对激动剂诱导的兔主动脉细胞内钙离子释放的影响。在含2 mM乙二醇双(β-氨基乙基醚)-N，N‘-四乙酸(EGTA-PSS)的无钙生理盐溶液中，用激动剂诱导的时相收缩作为细胞内钙释放的指示剂。在EGTA-PSS暴露期间，在组织中加入AP II(10(-9)-10(-7)M)15分钟，可剂量依赖性地抑制去甲肾上腺素(NE；10(-6)M)诱导的时相收缩。APⅡ的半最大抑制浓度为3×10~(-9)M，其中10×10~(-7)M的APⅡ的抑制率为91%。研究AP II(10(-7)M)对去甲肾上腺素(NE)刺激的45Ca外流的抑制作用证实了这一点。此外，组胺(10(-5)M)和咖啡因(25 MM)与去甲肾上腺素(NE)共同存在的细胞内钙释放也被AP II抑制。因此，AP II似乎是一种有效的抑制细胞内钙释放的药物，这种细胞内钙释放被多种激动剂用来激活血管平滑肌。这可能是AP II产生血管松弛的一个重要机制。

The effects of a synthetic atrial peptide (atriopeptin II; AP II) on the agonist-induced intracellular Ca2+ release was examined in the isolated rabbit aorta. The agonist-induced phasic contraction in a Ca2+-free physiological salt solution containing 2 mM ethyleneglycol-bis(beta-aminoethyl-ether)-N,N'-tetraacetic acid (EGTA-PSS) was used as an indicator of the intracellular Ca2+ release. The addition of AP II (10(-9)-10(-7) M) for 15 min to the tissue during the EGTA-PSS exposure caused a dose-dependent inhibition of norepinephrine (NE; 10(-6) M)-induced phasic contraction. The half-maximal inhibiting concentration of AP II was 3 X 10(-9) M, with 10(-7) M AP II causing 91% inhibition. This was confirmed by studying the inhibitory effect of AP II (10(-7) M) on NE-stimulated 45Ca efflux. Furthermore, the internal Ca2+ release by histamine (10(-5) M) and caffeine (25 mM), both of which share this internal Ca2+ pool with NE, was also inhibited by AP II. Thus AP II appears to be a potent inhibitor of the intracellular Ca2+ release that is utilized by various agonists for the activation of vascular smooth muscle. This may be an important mechanism by which AP II produces relaxation of blood vessels.

Atrial natriuretic factor elicits an endothelium-independent relaxation and activates particulate guanylate cyclase in vascular smooth muscle.