Parallel stimulation of glucose and Mg(2+) accumulation by insulin in rat hearts and cardiac ventricular myocytes.
The stimulation of beta-adrenoceptors in cardiac cells results in a rapid loss of cellular Mg(2+). Because insulin physiologically counteracts several of the cellular effects mediated by the activation of beta-adrenoceptors and the elevation of cytosolic cAMP levels, we investigated whether insulin administration could prevent Mg(2+) mobilization from rat hearts and ventricular myocytes. Rat hearts were perfused in a retrograde Langendorff system, and the changes in extracellular Mg(2+) were measured by atomic absorbance spectrophotometry. Pretreatment of the hearts with 6 nmol/L insulin completely prevented the Mg(2+) extrusion induced by the beta-adrenergic agonist isoproterenol. Furthermore, the administration of insulin per se induced an accumulation of Mg(2+) by the heart. This accumulation was small but detectable in the presence of 25 to 35 micromol/L [Mg(2+)](o) and increased in proportion to [Mg(2+)](o). Insulin-mediated Mg(2+) accumulation was not observed in hearts perfused with a medium devoid of glucose or with a medium containing the inhibitors of glucose transport, cytochalasin B and phloretin. Insulin-stimulated [(3)H]2-deoxyglucose accumulation was measured in collagenase-dispersed cardiac ventricular myocytes in the presence of varying levels of [Mg(2+)](o). Glucose transport was not observed below 25 micromol/L [Mg(2+)](o), and it also increased in proportion to [Mg(2+)](o). Taken together, these results indicate the presence of a major uptake of Mg(2+) into cardiac cells that is stimulated by insulin and may require the insulin-induced operation of a glucose transporter. Hence, extracellular and/or intracellular Mg(2+) may modulate glucose transport and/or utilization.
Romani
A M
AM
Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106-4970, USA. amr5@po.cwru.edu
Matthews
V D
VD
Scarpa
A
A
D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D003571:Cytochalasin B / Q000494:pharmacology; D003847:Deoxyglucose / Q000493:pharmacokinetics; D005947:Glucose / Q000378:metabolism*; D006352:Heart Ventricles; D066298:In Vitro Techniques; D007328:Insulin / Q000494:pharmacology*; D007545:Isoproterenol / Q000494:pharmacology; D008274:Magnesium / Q000378:metabolism*; D008297:Male; D009004:Monosaccharide Transport Proteins / Q000037:antagonists & inhibitors / Q000502:physiology; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D010693:Phloretin / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley
D000318:Adrenergic beta-Agonists; D007328:Insulin; D009004:Monosaccharide Transport Proteins; D003571:Cytochalasin B; D003847:Deoxyglucose; D008274:Magnesium; D005947:Glucose; D007545:Isoproterenol; D010693:Phloretin