HYPOMAGNESEMIA AND VASOCONSTRICTION - POSSIBLE RELATIONSHIP TO ETIOLOGY OF SUDDEN-DEATH ISCHEMIC-HEART-DISEASE AND HYPERTENSIVE VASCULAR DISEASES

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  • 1 January 1981
    • journal article
    • research article
    • Vol. 9  (3) , 212-231
Abstract
In vitro experiments are presented which indicate that the concentration of extracellular Mg 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 [dog, rat, pig], including man. Hypomognesemia 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 the [Mg2+]o can control the entry, distribution and exit of Ca ions (Ca2+) form 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, mellitus) are associated with a Mg-deficiency. [Mg2+]o and membrane Mg may play critical roles in regulating vascular tone and homeostasis.