6533b7d6fe1ef96bd1267219
RESEARCH PRODUCT
Modulatory role of magnesium on the contractile response of rat aorta to several agonists in normal and calcium-free medium.
M. Antonia NogueraM. Pilar D'oconsubject
Malemedicine.medical_specialtyContraction (grammar)Muscle RelaxationPharmaceutical Sciencechemistry.chemical_elementAorta ThoracicCalciumIn Vitro TechniquesMuscle Smooth VascularDivalentPotassium ChlorideNorepinephrineInternal medicinemedicineExtracellularAnimalsMagnesiumRats WistarPharmacologychemistry.chemical_classificationAcetylcholineCulture MediaRatsKineticsMuscle relaxationEndocrinologychemistryCalciummedicine.symptomIsotonic SolutionsExtracellular SpaceMagnesium DeficiencyVasoconstrictionAcetylcholinemedicine.drugMuscle contractionMuscle Contractiondescription
Abstract Acute withdrawal of external Mg2+ increased basal tone of rat isolated aorta incubated in the presence of Ca2+. Above normal levels of Mg2+ (1–4 Mm) inhibited basal tone while much higher levels of the divalent cation (64–256 Mm) evoked contractile responses regardless of the presence of Ca2+. Contractile responses to noradrenaline (1μm) and KCl (80 Mm) were inhibited by addition of cumulative concentrations of Mg2+. Acetylcholine-induced contractions in the presence of physiological concentrations of Mg2+ (1 Mm) decreased gradually to the basal tone, but a sustained contraction was observed in the absence of this ion. In Ca2+-free medium, acetylcholine-induced phasic responses indicate the existence of an acetylcholine-sensitive Ca2+ store. KCl induced contraction only in Krebs solution, although a small residual contraction could be observed in Ca2+-free medium in some experiments. Mg2+-depletion in the extracellular medium increased contractile responses induced by acetylcholine and KCl in Ca2+-free medium. These results suggest that extracellular Mg2+ modulates basal tone, Ca2+ channels and responsiveness to various agents in the absence of Ca2+.
year | journal | country | edition | language |
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1993-08-01 | The Journal of pharmacy and pharmacology |