Quamme G A, Rabkin S W
Department of Medicine, University of British Columbia University Hospital, Vancouver, Canada.
Biochem Biophys Res Commun. 1990 Mar 30;167(3):1406-12. doi: 10.1016/0006-291x(90)90679-h.
Regulation of intracellular Mg2+ activity in the heart is not well characterized. Cardiac myocytes were prepared as primary cultures from 7 day old chick embryo hearts and intracellular Mg2+ concentration [( Mg2+]i) was determined in single ventricular cells with mag-fura-2. Basal [Mg2+]i was 0.48 +/- 0.03 mM in normal culture medium. There was no correlation of basal [Mg2+]i with cellular contraction or intracellular [Ca2+]i (determined with fura-2). Cardiocytes cultured (16 hr) in low Mg (0.16 mM) media contained 0.21 +/- 0.05 mM Mg2+ which returned to normal levels when placed in Mg media with a refill time of 20 min. Basal [Ca2+]i (121 +/- 11 nM) and stimulated [Ca2+]i (231 +/- 41 nM) was similar to control cells. Verapamil, 25 microM, reversibly blocked Mg2+ refill. In conclusion, the basal [Mg2+]i of isolated cardiomyocytes is considerably below the Mg2+ electrochemical equilibrium allowing passive Mg2+ influx. The influx pathway for Mg2+ is inhibited by verapamil and appears to be independent of Ca2+ as assessed by fura-2.
心脏细胞内镁离子(Mg2+)活性的调节尚未得到充分研究。从7日龄鸡胚心脏制备原代培养的心肌细胞,并用mag-fura-2测定单个心室细胞内的镁离子浓度[Mg2+]i。在正常培养基中,基础[Mg2+]i为0.48±0.03 mM。基础[Mg2+]i与细胞收缩或细胞内钙离子浓度[Ca2+]i(用fura-2测定)之间没有相关性。在低镁(0.16 mM)培养基中培养16小时的心肌细胞含有0.21±0.05 mM的Mg2+,当置于含镁培养基中时,20分钟内可恢复到正常水平。基础[Ca2+]i(121±11 nM)和刺激后的[Ca2+]i(231±41 nM)与对照细胞相似。25 μM的维拉帕米可可逆地阻断Mg2+的再填充。总之,分离的心肌细胞的基础[Mg2+]i远低于Mg2+电化学平衡,允许Mg2+被动内流。Mg2+的内流途径受维拉帕米抑制,并且如用fura-2评估的那样,似乎独立于Ca2+。