New perspectives on the role of magnesium in the pathophysiology of the cardiovascular system. II. Experimental aspects.
It has generally been believed that the physiological roles for magnesium ions (Mg2+) in cardiac and vascular smooth muscle are limited to regulation of contractile proteins, sarcoplasmic reticular membrane transport of calcium ions (Ca2+), cofactor in ATPase activities and metabolic regulation of energy-dependent cytoplasmic and mitochondrial pathways. In addition, up until recently, it was not thought that small changes in free external ([Mg2+]0) or cytoplasmic Mg2+ could exert any significant effects on cardiac or vascular smooth muscle contractility. It is clear, however, from the newer studies that [Mg2+]0 can affect tension and contractility of these muscle cells by altering membrane and intracellular organelle binding and transport of Ca2+, affecting hormone-receptor interactions, regulating electrolyte content and transport, affecting resting membrane-generated and action potentials, altering excitation-contraction coupling events, and regulate peripheral and cerebral vascular tone and blood flow. In addition, it is also now clear that small changes of free [Mg2+] at the cardiac and vascular muscle membranes can exert significant effects on mechanical and electrical activities of these cells. Considerable new data lend support to the idea that [Mg2+]0 is fundamental in the regulation of cardiovascular homeostasis. Dietary, metabolic or drug-induced changes in Mg2+ levels appear to play important roles in the etiology of cardiac and vascular disorders. Evidence is reviewed and presented to indicate that Mg2+ is important in the pathophysiology and treatment of certain forms of experimental and genetic types of hypertension. This divalent cation may also be important in the etiology of a variety of disorders which have vasospasm in common. Evidence is reviewed to support the concept that Mg2+ is a naturally occurring or mimic weak Ca2+ antagonist, which should be useful in the treatment of several types of cardiac and vascular disorders.
D000818:Animals; D001692:Biological Transport; D001775:Blood Circulation; D001794:Blood Pressure / Q000187:drug effects; D002118:Calcium / Q000037:antagonists & inhibitors / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism; D002320:Cardiovascular Physiological Phenomena; D002560:Cerebrovascular Circulation; D003327:Coronary Disease / Q000209:etiology; D003329:Coronary Vasospasm / Q000209:etiology; D003331:Coronary Vessels / Q000187:drug effects; D003920:Diabetes Mellitus / Q000209:etiology; D004285:Dogs; D006168:Guinea Pigs; D006439:Hemodynamics / Q000187:drug effects; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000209:etiology; D008274:Magnesium / Q000097:blood / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology* / Q000627:therapeutic use; D008275:Magnesium Deficiency / Q000150:complications; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular / Q000378:metabolism; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D011817:Rabbits; D051381:Rats
D008274:Magnesium; D011188:Potassium; D002118:Calcium