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Role of Magnesium and Calcium in Alcohol‐Induced Hypertension and Strokes as Probed by In Vivo Television Microscopy, Digital Image Microscopy, Optical Spectroscopy, 31 P‐NMR, Spectroscopy and a Unique Magnesium Ion‐Selective Electrode
Author(s) -
Altura Burton M.,
Altura Bella T.
Publication year - 1994
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1994.tb00082.x
Subject(s) - spectroscopy , microscopy , magnesium , nuclear magnetic resonance spectroscopy , optical microscope , calcium , materials science , chemistry , optics , stereochemistry , physics , scanning electron microscope , metallurgy , quantum mechanics , composite material
It is not known why alcohol ingestion poses a risk for development of hypertension, stroke and sudden death. Of all drugs, which result in body depletion of magnesium (Mg), alcohol is now known to be the most notorious cause of Mg‐wasting. Recent data obtained through the use of biophysical (and noninvasive) technology suggest that alcohol may induce hypertension, stroke, and sudden death via its effects on intracellular free Mg 2+ ([Mg 2+ ]), which in turn alter cellular and subcellular bioenergetics and promote calcium ion (Ca 2+ ) overload. Evidence is reviewed that demonstrates that the dietary intake of Mg modulates the hypertensive actions of alcohol. Experiments with intact rats indicates that chronic ethanol ingestion results in both structural and hemodynamic alterations in the microcirculation, which, in themselves, could account for increased vascular resistance. Chronic ethanol increases the reactivity of intact microvessels to vasoconstrictors and results in decreased reactivity to vasodilators. Chronic ethanol ingestion clearly results in vascular smooth muscle cells that exhibit a progressive increase in exchangeable and cellular Ca 2+ concomitant with a progressive reduction in Mg content. Use of 31 P‐NMR spectroscopy coupled with opticalbackscatter reflectance spectroscopy revealed that acute ethanol administration to rats results in dose‐dependent deficits in phosphocreatine (PCr), the [PCr]/[ATP] ratio, intracellular pH (pH i ), oxyhemoglobin, and the mitochondrial level of oxidized cytochrome oxidase aa 3 concomitant with a rise in brain‐blood volume and inorganic phosphate. Temporal studies performed in vivo, on the intact brain, indicate that [Mg 2+ ], is depleted before any of the bioenergetic changes. Pretreatment of animals with Mg 2+ prevents ethanol from inducing stroke and prevents all of the adverse bioenergetic changes from taking place. Use of quantitative digital imaging microscopy, and mag‐fura‐2, on single‐cultured canine cerebral vascular smooth muscle, human endothelial, and rat astrocyte cells reveals that alcohol induces rapid concentration‐dependent depletion of [Mg 2+ ], These cellular deficits in [Mg 2+ ], seem to precipitate cellular and subcellular disturbances in cytoplasmic and mitochondrial bioenergetic pathways leading to Ca 2+ overload and ischemia. A role for ethanol‐induced alterations in [Mg 2+ ], should also be considered in the well‐known behavioral actions of alcohol.