ATRIONATRIURETIC-PEPTIDE TRANSFORMS CARDIAC SODIUM-CHANNELS INTO CALCIUM-CONDUCTING CHANNELS
ATRIONATRIURETIC-PEPTIDE TRANSFORMS CARDIAC SODIUM-CHANNELS INTO CALCIUM-CONDUCTING CHANNELS
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DOI：
10.1126/science.2154853
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发表时间：
1990-02-23
期刊：
影响因子：
56.9
通讯作者：
MORAD, M
中科院分区：
文献类型：
--
作者：
SORBERA, LA;MORAD, M
心房钠尿肽（ANP）在细胞外液容量增加的情况下从心房细胞释放，减少肾脏对钠的吸收，从而减少血容量。在本报告中，ANP抑制大鼠和豚鼠心室肌细胞的钙和钠电流。钠电流的抑制是由于钠通道对钙的渗透性增强而引起的，而钠通道的动力学和河豚毒素敏感性没有显著变化。因此，ANP可能通过改变其对钙离子的阳离子选择性位点来调节钠离子通道，从而抑制钠离子电流。钠和钙通道的抑制以及由此导致的心房细胞兴奋性的抑制可能有助于调节ANP的分泌。
The atrionatriuretic peptide (ANP) is released from atrial cells in response to increased extracellular fluid volume and reduces sodium absorption by the kidney, thus reducing the blood volume. In this report, ANP suppressed the calcium and sodium currents in rat and guinea pig ventricular myocytes. The suppression of sodium current was caused by enhanced permeability of the sodium channel to calcium without significant changes in the kinetics or the tetrodotoxin sensitivity of the channel. Thus, ANP may regulate the sodium channel by altering its cationic selectivity site to calcium, thereby repressing the sodium current. The suppression of sodium and calcium channels and the resultant depressed excitability of the atrial cells may help to regulate ANP secretion.