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      Magnesium and Vascular Tone and Reactivity


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          It has been reported that the concentration of extracellular magnesium ions ([Mg<sup>++</sup>]<sub>o</sub>) can affect blood flow, blood pressure and vascular reactivity in intact mammals. The present studies, using a variety of rat and rabbit blood vessels, were undertaken to shed further light on the relationship between [Mg<sup>++</sup>]<sub>o</sub>, Ca<sup>++</sup>, tone and vascular responsiveness. [Mg<sup>++</sup>]<sub>o</sub> was found to differentially affect a variety of hormone and drug-induced contractions in isolated rat and rabbit arteries as well as isolated perfused rat mesenteric arterioles (15–20 µm i.d.). Progressive elevations in [Mg<sup>++</sup>]<sub>o</sub> above physiologic levels will dose-dependently produce progressive, increased inhibition of most contractile substances. These results are not reflections of osmolarity. Withdrawal of [Mg<sup>++</sup>]<sub>o</sub> can induce contractions of rat arteries as well as of isolated perfused rat mesenteric arterioles. Using isolated rat portal veins, withdrawal of [Mg<sup>++</sup>] results in rapid enhancement of the spontaneously evoked mechanical responses and increases in rhythmic contractility; these spontaneously evoked responses are abolished in hypermagnesemic solutions (e.g., 10 mM). The contractile responses observed upon withdrawal of [Mg<sup>++</sup>]<sub>o</sub> are dependent upon the [Ca<sup>++</sup>] and the polarity of the membrane but are not related to inhibition of Na<sup>+</sup>, K<sup>+</sup> ATPase. With rat aortic strips, addition of CaEDTA potentiates contractions induced by Mg<sup>++</sup> withdrawal, while EGTA promotes rapid relaxations. Rapid relaxations of contractions induced by Mg<sup>++</sup> withdrawal in rat aorta could also be induced by Mn<sup>++</sup>, Ni<sup>++</sup>, Co<sup>++</sup> and Cd<sup>++</sup> but not Sr<sup>++</sup>. Addition of [Ni<sup>++</sup>] to portal veins exposed either to a Mg<sup>++</sup>-free solution, or to a solution containing Mg<sup>++</sup>, results in dose-dependent, and eventual complete, inhibition of all spontaneous mechanical events. These data suggest that [Mg<sup>++</sup>]<sub>o</sub>: (a) plays an important role in regulating membrane permeability to [Ca<sup>++</sup>]<sub>o</sub>; (b) probably occupies sites which are exchangeable with membrane-bound Ca in arterial, venous and arteriolar smooth muscle; (c) acts intracellularly as well to compete with Ca for certain divalent cation sites; and (d) may play an important role in regulating arteriolar tone and blood pressure.

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          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          18 September 2008
          : 15
          : 1-3
          : 5-16
          Department of Physiology, State University of New York, Downstate Medical Center, Brooklyn, N.Y.
          158148 Blood Vessels 1978;15:5–16
          © 1978 S. Karger AG, Basel

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          Page count
          Pages: 12
          Molecular and Cellular Aspects of Vascular Smooth Muscle in Health and Disease


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