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心房利钠肽与钙拮抗剂对培养的血管平滑肌细胞胞质游离钙影响的差异。

Difference between the effects of atrial natriuretic peptide and calcium antagonist on cytosolic free calcium in cultured vascular smooth muscle cells.

作者信息

Takeuchi K, Abe K, Yasujima M, Sato M, Kasai Y, Tsunoda K, Hagino T, Kanazawa M, Yoshinaga K

机构信息

Second Department of Internal Medicine, Tohoku University, School of Medicine, Sendai, Japan.

出版信息

J Cardiovasc Pharmacol. 1989;13 Suppl 6:S13-6.

PMID:2473340
Abstract

The effect of atrial natriuretic peptide (ANP) on cytosolic free calcium ([Ca2+]i) was studied in monolayers of cultured vascular smooth muscle (VSM) cells loaded with a fluorescent calcium indicator, fura-2. ANP (atriopeptin III, 10(-8) M) decreased the resting level of [Ca2+]i and sustained rises in [Ca2+]i following peak levels induced by vasoconstrictive hormones (angiotensin II or vasopressin). ANP also decreased a rise in [Ca2+]i induced by high potassium (high K+) depolarization. The initial rise in [Ca2+]i induced by vasopressin was not inhibited by ANP. On the other hand, calcium antagonists (nicardipine or nifedipine) inhibited the high K+-induced rise in [Ca2+]i, whereas there was no effect on rises in [Ca2+]i induced by vasopressin. These results suggest that calcium antagonists inhibit voltage-dependent calcium channels, while ANP can decrease [Ca2+]i presumably through a stimulation of calcium-extrusion active transports in vascular smooth muscle cells.

摘要

利用荧光钙指示剂fura - 2负载培养的血管平滑肌(VSM)细胞单层,研究了心房利钠肽(ANP)对胞质游离钙([Ca2 +]i)的影响。ANP(心房肽III,10(-8) M)降低了[Ca2 +]i的静息水平,并在血管收缩激素(血管紧张素II或血管加压素)诱导的峰值水平后持续升高[Ca2 +]i。ANP还降低了高钾(高K +)去极化诱导的[Ca2 +]i升高。血管加压素诱导的[Ca2 +]i初始升高不受ANP抑制。另一方面,钙拮抗剂(尼卡地平或硝苯地平)抑制了高K +诱导的[Ca2 +]i升高,而对血管加压素诱导的[Ca2 +]i升高没有影响。这些结果表明,钙拮抗剂抑制电压依赖性钙通道,而ANP可能通过刺激血管平滑肌细胞中的钙排出主动转运来降低[Ca2 +]i。

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