title: Hypomagnesemia and vasoconstriction: possible relationship to etiology of sudden death ischemic heart disease and hypertensive vascular diseases.
abstract: In-vitro experiments are presented which indicate that the concentration of extracellular magnesium ions ([Mg2+]o) can exert profound influences on the contractility and reactivity of arteries, arterioles and veins from a number of regional vasculatures in several mammalian species, including man. Hypomagnesemia can potentiate the contractile activity of a variety of neurohumoral substances and induce vasospasm. Hypermagnesemia can do the reverse, i.e., induce hyporeactivity, relaxation and vasodilatation. Data are also presented to indicate that [Mg2+]o can control the entry, distribution and exit of calcium ions (Ca2+) from vascular smooth muscle cells. Arterial and venous smooth muscles excised from rats with alloxan-diabetes mellitus or spontaneous hypertension (SHR) appear to exhibit vascular membranes which have modifications in their Mg-Ca exchange sites. Data are reviewed which suggest that certain vascular diseases (e.g., sudden-death ischemic heart disease, hypertension, eclampsia, diabetes mellitus) are associated with a Mg-deficiency. Overall, it is suggested that [Mg2+]o and membrane [Mg] may play critical roles in regulating vascular tone and homeostasis.
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D002463:Cell Membrane Permeability; D003327:Coronary Disease / Q000209:etiology*; D003645:Death, Sudden / Q000209:etiology*; D003920:Diabetes Mellitus / Q000378:metabolism; D004285:Dogs; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism; D066298:In Vitro Techniques; D008274:Magnesium / Q000378:metabolism; D008275:Magnesium Deficiency / Q000150:complications*; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D013552:Swine; D014661:Vasoconstriction / Q000187:drug effects*
chemical_list: D008274:Magnesium; D011188:Potassium; D002118:Calcium