TY - JOUR
T1 - Effects of extracellular magnesium and beta adrenergic stimulation on contractile force and magnesium mobilization in the isolated rat heart.
AU - Howarth, F. C.
AU - Waring, J.
AU - Hustler, B. I.
AU - Singh, J.
PY - 1994/12
Y1 - 1994/12
N2 - This study investigates the metabolism of the divalent cation, magnesium (Mg2+) in the isolated perfused Langendorff's rat heart and ventricular slices in the absence and presence of catecholamines including isoprenaline, noradrenaline and adrenaline. Perfusion of the isolated rat heart with a physiological salt solution containing elevated extracellular Mg2+ [Mg2+]o (2.4 mM-6.0 mM) resulted in a marked and progressive decrease in the amplitude of contraction compared to control [Mg2+]o (1.2 mM). In contrast, perfusion of hearts with low (0-0.6 mM) [Mg2+]o caused a small transient increase in the amplitude of contraction which was often accompanied by arrhythmic activity. Perfusion of the heart with a nominally Mg2+ free medium resulted in a time-dependent net efflux of Mg2+ reaching a steady state after approximately 40-50 min of perfusion. This release of Mg2+ was associated with a concurrent decrease in total heart Mg2+. Stimulation of the heart with the beta adrenergic agonist, isoprenaline (10(-7) M) caused large increases in net Mg2+ efflux which was associated with marked increased in both rate and the amplitude of contraction. Similar effects on Mg2+ efflux were also observed during perfusion of the heart with the adenylate cyclase activator, forskolin (10(-5) M). Superfusion of paced ventricular segments with either isoprenaline, adrenaline or noradrenaline (all 10(-6) M) also resulted in a marked transient net efflux of Mg2+. Pre-treatment of segments with the beta adrenergic antagonist, propranolol (10(-5) M) competitively blocked the Mg2+ efflux evoked by the catecholamines. Similarly, pre-treatment of segments with the calcium (Ca2+) channel blocker, verapamil (10(-5) M) caused a significant (P < 0.05) decrease in net Mg2+ efflux evoked by isoprenaline. The results of this study indicate that (1) the perturbation of [Mg2+]o has an important influence on myocardial contractility and (2) the mobilization of Mg2+ in the heart is associated with beta adrenergic stimulation possibly via an elevation in intracellular adenosine 3.5 cyclic monophosphate (cyclic AMP).
AB - This study investigates the metabolism of the divalent cation, magnesium (Mg2+) in the isolated perfused Langendorff's rat heart and ventricular slices in the absence and presence of catecholamines including isoprenaline, noradrenaline and adrenaline. Perfusion of the isolated rat heart with a physiological salt solution containing elevated extracellular Mg2+ [Mg2+]o (2.4 mM-6.0 mM) resulted in a marked and progressive decrease in the amplitude of contraction compared to control [Mg2+]o (1.2 mM). In contrast, perfusion of hearts with low (0-0.6 mM) [Mg2+]o caused a small transient increase in the amplitude of contraction which was often accompanied by arrhythmic activity. Perfusion of the heart with a nominally Mg2+ free medium resulted in a time-dependent net efflux of Mg2+ reaching a steady state after approximately 40-50 min of perfusion. This release of Mg2+ was associated with a concurrent decrease in total heart Mg2+. Stimulation of the heart with the beta adrenergic agonist, isoprenaline (10(-7) M) caused large increases in net Mg2+ efflux which was associated with marked increased in both rate and the amplitude of contraction. Similar effects on Mg2+ efflux were also observed during perfusion of the heart with the adenylate cyclase activator, forskolin (10(-5) M). Superfusion of paced ventricular segments with either isoprenaline, adrenaline or noradrenaline (all 10(-6) M) also resulted in a marked transient net efflux of Mg2+. Pre-treatment of segments with the beta adrenergic antagonist, propranolol (10(-5) M) competitively blocked the Mg2+ efflux evoked by the catecholamines. Similarly, pre-treatment of segments with the calcium (Ca2+) channel blocker, verapamil (10(-5) M) caused a significant (P < 0.05) decrease in net Mg2+ efflux evoked by isoprenaline. The results of this study indicate that (1) the perturbation of [Mg2+]o has an important influence on myocardial contractility and (2) the mobilization of Mg2+ in the heart is associated with beta adrenergic stimulation possibly via an elevation in intracellular adenosine 3.5 cyclic monophosphate (cyclic AMP).
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M3 - Article
C2 - 7786682
AN - SCOPUS:0028709002
SN - 0953-1424
VL - 7
SP - 187
EP - 197
JO - Magnesium research : official organ of the International Society for the Development of Research on Magnesium
JF - Magnesium research : official organ of the International Society for the Development of Research on Magnesium
IS - 3-4
ER -