Na-dependent Regulation of Intracellular Free Magnesium Concentration in Isolated Rat Ventricular Myocytes

• Published in: Journal of molecular and cellular cardiology Vol. 28; no. 8; pp. 1641 - 1651
• Main Authors: Handy, R.D., Gow, I.F., Ellis, D., Flatman, P.W.
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01-08-1996
• Subjects: Animals; Antiporters - physiology; Heart Ventricles - cytology; Heart Ventricles - drug effects; Heart Ventricles - metabolism; Homeostasis; Imipramine; Imipramine - pharmacology; In Vitro Techniques; Intracellular free magnesium; Ion Channels - antagonists & inhibitors; Mag-fura-2; Magnesium; Magnesium - metabolism; Magnesium transport; Male; Na–Mg antiport; Rat ventricular myocyte; Rats; Rats, Sprague-Dawley; Reproducibility of Results; Sodium - metabolism; Statistics as Topic; Strophanthidin; Strophanthidin - pharmacology; Verapamil; Verapamil - pharmacology; Strophanthidin; Imipramine; Rat ventricular myocyte; Mag-fura-2; Verapamil; Magnesium; Magnesium transport; Intracellular free magnesium; Na–Mg antiport
• ISSN: 0022-2828; 1095-8584
• DOI: 10.1006/jmcc.1996.0154

Changes in ionized intracellular free magnesium concentration [Mg
2+]
iwere measured in isolated, superfused rat ventricular myocytes using mag-fura-2. Cells were superfused with media containing high or low Mg concentrations ( [Mg]
0), with and without Na (Na
0) and/or Ca (Ca
0). Increasing [Mg]
0from 1 to 5 mmol/l in Ca-free solutions had no significant effect on [Mg
2+]
iwhen [Na]
0was normal. However, [Mg
2+]
irose steadily when Na
0was completely replaced by either tetramethylammonium (TMA) or K. This [Mg
2+]
irise was inhibited by imipramine (10
μmol/l) but not by verapamil (25
μmol/l). [Mg
2+]
ireturned rapidly from a high to its initial level on superfusing cells with basic medium containing normal Ca, Na and Mg. [Mg
2+]
irecovery required Na
0and was inhibited by imipramine (10
μmol/l). When Mg
0was removed from Ca-free superfusates, the [Mg
2+]
idecreased whether or not Na
0was present. However, [Mg
2+]
idecreased most when Na
0was replaced by K. Neither imipramine nor verapamil affected the magnitude of this fall, but verapamil slowed it. [Mg
2+]
irapidly increased to normal when depleted cells were superfused with basic medium with or without Ca
0. Both imipramine and verapamil slowed this recovery. Superfusion of cells with Ca-free media containing strophanthidin (20
μmol/l) caused [Mg
2+]
ito rise, but only if the medium contained Mg (1 mmol/l). The data suggest that Mg can enter cardiac myocytes through routes which close when physiological [Mg
2+]
iis attained. One pathway for Mg flux is by a Na-dependent, imipramine-sensitive mechanism which is probably a Na–Mg antiport.