Takeuchi K, Abe K, Yasujima M, Sato M, Kasai Y, Tsunoda K, Hagino T, Kanazawa M, Yoshinaga K
Second Department of Internal Medicine, Tohoku University, School of Medicine, Sendai, Japan.
J Cardiovasc Pharmacol. 1989;13 Suppl 6:S13-6.
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.
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。
