Cellular Biology |
From the Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio.
Correspondence to Andrea M.P. Romani, Department of Physiology and Biophysics, Case Western Reserve University, 10900 Euclid Ave, Cleveland, OH 44106-4970. E-mail amr5{at}po.cwru.edu
AbstractThe stimulation of ß-adrenoceptors in cardiac cells results in a rapid loss of cellular Mg2+. Because insulin physiologically counteracts several of the cellular effects mediated by the activation of ß-adrenoceptors and the elevation of cytosolic cAMP levels, we investigated whether insulin administration could prevent Mg2+ mobilization from rat hearts and ventricular myocytes. Rat hearts were perfused in a retrograde Langendorff system, and the changes in extracellular Mg2+ were measured by atomic absorbance spectrophotometry. Pretreatment of the hearts with 6 nmol/L insulin completely prevented the Mg2+ extrusion induced by the ß-adrenergic agonist isoproterenol. Furthermore, the administration of insulin per se induced an accumulation of Mg2+ by the heart. This accumulation was small but detectable in the presence of 25 to 35 µmol/L [Mg2+]o and increased in proportion to [Mg2+]o. Insulin-mediated Mg2+ 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 [3H]2-deoxyglucose accumulation was measured in collagenase-dispersed cardiac ventricular myocytes in the presence of varying levels of [Mg2+]o. Glucose transport was not observed below 25 µmol/L [Mg2+]o, and it also increased in proportion to [Mg2+]o. Taken together, these results indicate the presence of a major uptake of Mg2+ into cardiac cells that is stimulated by insulin and may require the insulin-induced operation of a glucose transporter. Hence, extracellular and/or intracellular Mg2+ may modulate glucose transport and/or utilization.
Key Words: Mg2+ cardiac myocytes hearts insulin glucose transport
This article has been cited by other articles:
![]() |
R. M. Touyz Transient receptor potential melastatin 6 and 7 channels, magnesium transport, and vascular biology: implications in hypertension Am J Physiol Heart Circ Physiol, March 1, 2008; 294(3): H1103 - H1118. [Abstract] [Full Text] [PDF] |
||||
![]() |
P Delva, M Degan, M Trettene, and A Lechi Insulin and glucose mediate opposite intracellular ionized magnesium variations in human lymphocytes. J. Endocrinol., September 1, 2006; 190(3): 711 - 718. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. M. Torres, J. Youngner, and A. Romani Role of glucose in modulating Mg2+ homeostasis in liver cells from starved rats Am J Physiol Gastrointest Liver Physiol, February 1, 2005; 288(2): G195 - G206. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Young, C. Cefaratti, and A. Romani Chronic EtOH administration alters liver Mg2+ homeostasis Am J Physiol Gastrointest Liver Physiol, January 1, 2003; 284(1): G57 - G67. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Shi and J. Cui Intracellular Mg2+ Enhances the Function of Bk-Type Ca2+-Activated K+ Channels J. Gen. Physiol., November 1, 2001; 118(5): 589 - 606. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. E. Fagan and A. Romani Activation of Na+- and Ca2+-dependent Mg2+ extrusion by alpha 1- and beta -adrenergic agonists in rat liver cells Am J Physiol Gastrointest Liver Physiol, November 1, 2000; 279(5): G943 - G950. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Murphy Mysteries of Magnesium Homeostasis Circ. Res., February 18, 2000; 86(3): 245 - 248. [Full Text] [PDF] |
||||
![]() |
R. M. Touyz, C. Mercure, and T. L. Reudelhuber Angiotensin II Type I Receptor Modulates Intracellular Free Mg2+ in Renally Derived Cells via Na+-dependent Ca2+-independent Mechanisms J. Biol. Chem., April 20, 2001; 276(17): 13657 - 13663. [Abstract] [Full Text] [PDF] |
||||
|
Circulation Research Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2000 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |