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Magnesium deficiency produces endothelium-dependent vasorelaxation in canine coronary arteries.

Abstract
In the present study, effects of magnesium deficiency on coronary vascular reactivity changes were studied in isolated canine coronary arteries before and after endothelium disruption. Lowering of extracellular magnesium produced a potent vasorelaxant response in coronary arteries with intact endothelium, whereas in arteries with disrupted endothelium a potent vasoconstrictory response was observed. The magnitude of magnesium deficiency-induced vasorelaxation is also dependent on the extracellular calcium concentrations, such that lowering of extracellular calcium from 1.75 to 0.22 mM completely abolished the magnesium deficiency-induced vasorelaxant effects. Similar inhibition, as well as reversal, of magnesium deficiency-induced vasorelaxation was also observed with dichlorobenzamil, a known inhibitor of the Na+/Ca++ exchange mechanism, but not with nifedipine, a known inhibitor of the voltage-operated calcium channel. The magnesium deficiency-induced vasoconstriction, on the other hand, is endothelium-independent. Although a similar dependency on extracellular calcium concentration was observed in this vasoconstrictory response, nifedipine, but not dichlorobenzamil, was found to be effective in inhibiting the vasoconstrictory effect. Hemoglobin, a known inhibitor of the endothelium-derived relaxing factor, also completely inhibited the magnesium deficiency-induced vasorelaxation but had no effect on the latter vasoconstrictory effect. These results suggest that circulating magnesium ion may have a dual effect in the modulation of coronary vascular reactivity. In coronary vessels with intact endothelium, lowering of extracellular magnesium may potentiate calcium-induced basal release of endothelium-derived relaxing factor and result in vasodilation, whereas in pathological vessels with injured endothelial cells, a similar lowering of magnesium may increase coronary vascular tone by accentuating the calcium-induced coronary constrictory response in vascular smooth muscle cells and result in vasoconstriction.
AuthorsD D Ku, H S Ann
JournalThe Journal of pharmacology and experimental therapeutics (J Pharmacol Exp Ther) Vol. 241 Issue 3 Pg. 961-6 (Jun 1987) ISSN: 0022-3565 [Print] UNITED STATES
PMID3598912 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • 3',4'-dichlorobenzamil
  • Amiloride
  • Nifedipine
Topics
  • Amiloride (analogs & derivatives, pharmacology)
  • Animals
  • Coronary Vessels (physiopathology)
  • Dogs
  • Endothelium (physiopathology)
  • Female
  • Magnesium Deficiency (physiopathology)
  • Male
  • Nifedipine (pharmacology)
  • Vasodilation

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