Magnesium, electrolyte transport and coronary vascular tone.
Coronary heart diseases (CHD) have high indices of mortality and morbidity. A number of CHD and myocardial ischaemic syndromes such as unstable angina pectoris, sudden death ischaemic heart disease, acute myocardial infarction and ventricular arrhythmias have been associated with losses of myocardial magnesium and potassium. Mg++ ions are essential for regulation of Na+ and K+ transport across cell membranes, including those found in cardiac and vascular smooth muscle cells. Mg++ activates an Na+-K+-ATPase pump which in turn plays a major role in regulating Na+-K+ transport. Loss of cellular Mg++ results in loss of critically important phosphagens: MgATP and creatine phosphate. Thus, under conditions where cellular Mg++ is depleted (e.g. hypoxia, ischaemia, anoxia), the Na+-K+ pump and phosphagen stores will be compromised, leading to alterations in resting membrane potentials. Cellular Mg++ depletion has been found to result in concomitant depletion of K+ in a number of cells, including cardiac and vascular muscles. The consequences of these events are often production of cardiac arrhythmias. Myocardial and vascular injury lead to disturbances in electrolyte transport across cell membranes, whereby Na+ and Ca++ uptakes are enhanced and, just prior or concomitantly, Mg++ and K+ are lost. Such electrolyte disturbances often lead to necrotic foci. Considerable evidence has accumulated to indicate that the extracellular concentration of Mg++ is important in control of arterial tone and blood pressure via pressure via regulation of vascular membrane Mg++-Ca++ exchange sites. A reduction in the extracellular Mg++ concentration can produce hypertension, coronary vasospasm and potentiation of vasoconstrictor agents by allowing excess entry of Ca++; concomitantly, the potency of vasodilator agents is reduced. Alterations in vascular membrane Mg++ results in arterial and arteriolar membranes which are 'leaky', thus contributing to the cellular reduction in K+ and gain of Na+ and Ca+. Alterations in extracellular K+ or Na+ concentrations over physiological ranges, in the face of a Mg++ deficit, can exacerbate the coronary vasospasm noted with reduction in only extracellular Mg++. Since free Mg++ ions are necessary for maintaining Ca+ ions (both plasma membrane-bound and sarcoplasmic reticulum membrane-bound via Ca++ ATPases), intracellular free Mg++ would rise in conditions which result in cellular loss of Mg++, thereby exacerbating and contributing to elevation of blood pressure and coronary vasospasm.(ABSTRACT TRUNCATED AT 400 WORDS)
D000818:Animals; D001693:Biological Transport, Active; D002463:Cell Membrane Permeability / Q000187:drug effects; D002784:Cholesterol / Q000097:blood; D003327:Coronary Disease / Q000503:physiopathology; D003331:Coronary Vessels / Q000502:physiology*; D000242:Cyclic AMP / Q000502:physiology; D004032:Diet; D004573:Electrolytes / Q000378:metabolism*; D006801:Humans; D008274:Magnesium / Q000378:metabolism / Q000502:physiology*; D008903:Minerals / Q000032:analysis; D018377:Neurotransmitter Agents / Q000502:physiology; D009994:Osmolar Concentration; D011188:Potassium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014652:Vascular Diseases / Q000503:physiopathology; D014881:Water Supply / Q000032:analysis
D004573:Electrolytes; D008903:Minerals; D018377:Neurotransmitter Agents; D002784:Cholesterol; D000242:Cyclic AMP; D000254:Sodium-Potassium-Exchanging ATPase; D008274:Magnesium; D011188:Potassium