Inhibition of sodium-calcium and sodium-proton exchangers by amiloride congeners in arterial muscle cells.
Inhibition of sodium-calcium and sodium-proton exchangers by amiloride congeners in arterial muscle cells.
复制标题
阿米洛利同系物对动脉肌细胞中钠-钙和钠-质子交换剂的抑制作用。
DOI：
10.1016/0006-2952(91)90633-g
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发表时间：
1991
影响因子：
5.8
通讯作者：
Smith,L
中科院分区：
文献类型：
--
作者：
Smith,JB;Lyu,RM;Smith,L
比较了几种阿米洛利同系物对大鼠主动脉肌细胞Na+-Ca 2+和Na+-H+交换的抑制作用。N-（2，4-二甲基苄基）阿米洛利（DMB）对Na+-Ca 2+交换的作用比Na+-H+交换强10倍.阿米洛利和乙基异丙基阿米洛利对Na+-H+的交换作用分别是Na+-Ca 2+交换作用的5,000倍和10,000倍. N-（3，4-二氯苄基）氨氯吡咪对两种交换剂的作用几乎相等。约40 nM乙基异丙基氨氯吡咪抑制Na+-H+交换50%。乙基异丙氨氯吡咪（10 μM）对基础或血管紧张素诱发的45 Ca 2+流出或净Ca 2+流出无影响。与乙基异丙氨氯吡咪相反，25-50 μM的DMB可显著抑制Na+-Ca 2+交换，使血管紧张素产生的45 Ca 2+流出和净Ca 2+流出均显著减少。用N-甲基-D-葡糖胺替代细胞外Na+，抑制血管紧张素诱导的45 Ca 2+外排，其作用与DMB相似。无论是DMB还是Na+的放置对基础或血管紧张素诱发的[3 H]肌醇磷酸的产生都没有任何影响。这些结果提示Na+-H+交换对短期Ca 2+调节无明显影响，并为Na+-Ca 2+交换是刺激后动脉肌细胞快速Ca 2+流出的主要途径提供了证据。
The inhibitory potencies of several amiloride congeners towards Na+-Ca 2+ and Na+-H+ exchange were compared in rat aortic myocytes. N-(2, 4-Dimethylbenzyl) amiloride (DMB) was 10 times more potent towards Na+-Ca 2+ than Na+-H+ exchange. Amiloride and ethylisopropylamiloride were about 5,000 and 10,000 times more potent towards Na+-H+ than Na+-Ca 2+ exchange respectively. N-(3, 4-Dichlorobenzyl) amiloride was almost equipotent towards both exchangers. About 40 nM ethylisopropylamiloride inhibited Na+-H+ exchange by 50%. Ethylisopropylamiloride (10 μM) had no effect on basal or angiotensin-evoked 45 Ca 2+ efflux or net Ca 2+ efflux. In contrast to ethylisopropylamiloride, 25–50 μM DMB, which strongly inhibits Na+-Ca 2+ exchange, markedly decreased both 45 Ca 2+ efflux and net Ca 2+ efflux produced by angiotensin. Replacing extracellular Na+ with N-methyl-D-glucamine inhibited angiotensin-evoked 45 Ca 2+ efflux similarly to DMB. Neither DMB nor Na+ placement had any effect on basal or angiotensin-evoked production of [3 H] inositol phosphates. These findings suggest that Na+-H+ exchange has no major influence on short-term Ca 2+ regulation and provide evidence that Na+-Ca 2+ exchange is a major pathway of rapid Ca 2+ efflux in stimulated arterial muscle cells.