This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Yoshimura, M. Articles by Kajiyama, G. Search for Related Content PubMed PubMed Citation Articles by Yoshimura, M. Articles by Kajiyama, G.

(Circulation. 1997;95:2567.)
© 1997 American Heart Association, Inc.

Articles

Extracellular Mg²⁺ Inhibits Capacitative Ca²⁺ Entry in Vascular Smooth Muscle Cells

Mitsuisa Yoshimura, MD; Tetsuya Oshima, MD; Hideo Matsuura, MD; Takafumi Ishida, MD; Masayuki Kambe, MD; Goro Kajiyama, MD

the First Department of Internal Medicine (M.Y., H.M., T.I., G.K.) and the Department of Clinical Laboratory Medicine (T.O., M.K.), Hiroshima (Japan) University School of Medicine.

Correspondence to Tetsuya Oshima, MD, Department of Clinical Laboratory Medicine, Hiroshima University School of Medicine, 1-2-3 Kasumi, Minami-ku, Hiroshima 734, Japan.

Abstract

Background Agonist-induced Ca²⁺ entry is thought to be mediated by capacitative Ca²⁺ entry other than L-type Ca²⁺ channels in vascular smooth muscle cells (VSMCs). The mechanism for capacitative Ca²⁺ entry has not been fully elucidated. Our objective was to examine the effect of external Mg²⁺ on capacitative Ca²⁺ entry in cultured rat aortic VSMCs.

Methods and Results Three doses of external Mg²⁺ concentration (nominally 0, 1, and 5 mmol/L) were used. After exposure to 1 µmol/L angiotensin II (Ang II) in Ca²⁺-free medium, addition of Ca²⁺ to the medium caused an increase in cytosolic free Ca²⁺ concentration ([Ca²⁺]_i), indicating Ang II–induced Ca²⁺ influx. This Ca²⁺ influx was attenuated in cells preincubated with high external Mg²⁺ concentrations or with 1 µmol/L nifedipine. After VSMCs in Ca²⁺-free medium were exposed to 1 µmol/L thapsigargin, which inhibits the sarcoplasmic reticulum Ca²⁺-ATPase and depletes Ca²⁺ stores, addition of Ca²⁺ to the medium induced an increase in [Ca²⁺]_i, indicating capacitative Ca²⁺ entry. This entry pathway was found to be independent of dihydropyridine-sensitive Ca²⁺ channels and inhibited by increased external Mg²⁺ concentration. External Mg²⁺ concentration did not influence Ca²⁺ efflux across the plasma membrane after stimulation with Ang II plus thapsigargin.

Conclusions Results suggest that in VSMCs, capacitative Ca²⁺ entry is reduced by external Mg²⁺. This mechanism may explain in part the inhibitory effect of external Mg²⁺ on Ca²⁺ handling.

Key Words: calcium • cells • muscle, smooth

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]

				J. Zhang, W. G. Wier, and M. P. Blaustein Mg2+ blocks myogenic tone but not K+-induced constriction: role for SOCs in small arteries Am J Physiol Heart Circ Physiol, December 1, 2002; 283(6): H2692 - H2705. [Abstract] [Full Text] [PDF]

				H Teragawa, M Kato, T Yamagata, H Matsuura, and G Kajiyama Magnesium causes nitric oxide independent coronary artery vasodilation in humans Heart, August 1, 2001; 86(2): 212 - 216. [Abstract] [Full Text] [PDF]

				H. Bouillier, E. Samain, C. Rucker-Martin, J.-F. Renaud, M. Safar, and G. Dagher Effect of Extracellular Matrix Elements on Angiotensin II-Induced Calcium Release in Vascular Smooth Muscle Cells From Normotensive and Hypertensive Rats Hypertension, June 1, 2001; 37(6): 1465 - 1472. [Abstract] [Full Text] [PDF]

				S. S. McDaniel, O. Platoshyn, J. Wang, Y. Yu, M. Sweeney, S. Krick, L. J. Rubin, and J. X.-J. Yuan Capacitative Ca2+ entry in agonist-induced pulmonary vasoconstriction Am J Physiol Lung Cell Mol Physiol, May 1, 2001; 280(5): L870 - L880. [Abstract] [Full Text] [PDF]

				H. Teragawa, M. Kato, T. Yamagata, H. Matsuura, and G. Kajiyama The Preventive Effect of Magnesium on Coronary Spasm in Patients With Vasospastic Angina Chest, December 1, 2000; 118(6): 1690 - 1695. [Abstract] [Full Text] [PDF]

				R. M. Touyz and E. L. Schiffrin Signal Transduction Mechanisms Mediating the Physiological and Pathophysiological Actions of Angiotensin II in Vascular Smooth Muscle Cells Pharmacol. Rev., December 1, 2000; 52(4): 639 - 672. [Abstract] [Full Text] [PDF]

				O. Stepien and P. Marche Amlodipine inhibits thapsigargin-sensitive CA2+ stores in thrombin-stimulated vascular smooth muscle cells Am J Physiol Heart Circ Physiol, September 1, 2000; 279(3): H1220 - H1227. [Abstract] [Full Text] [PDF]

				A. Arnon, J. M. Hamlyn, and M. P. Blaustein Ouabain augments Ca2+ transients in arterial smooth muscle without raising cytosolic Na+ Am J Physiol Heart Circ Physiol, August 1, 2000; 279(2): H679 - H691. [Abstract] [Full Text] [PDF]

				A. Arnon, J. M. Hamlyn, and M. P. Blaustein Na+ entry via store-operated channels modulates Ca2+ signaling in arterial myocytes Am J Physiol Cell Physiol, January 1, 2000; 278(1): C163 - C173. [Abstract] [Full Text] [PDF]

				E. Samain, H. Bouillier, S. Miserey, C. Perret, J.-F. Renaud, M. Safar, and G. Dagher Extracellular Signal-Regulated Kinase Pathway Is Involved in Basic Fibroblast Growth Factor Effect on Angiotensin II-Induced Ca2+ Transient in Vascular Smooth Muscle Cell From Wistar-Kyoto and Spontaneously Hypertensive Rats Hypertension, January 1, 2000; 35(1): 61 - 67. [Abstract] [Full Text] [PDF]

				M. J. Davis and M. A. Hill Signaling Mechanisms Underlying the Vascular Myogenic Response Physiol Rev, April 1, 1999; 79(2): 387 - 423. [Abstract] [Full Text] [PDF]

				M. Yoshimura, T. Oshima, H. Matsuura, T. Inoue, M. Kambe, and G. Kajiyama Differential Effects of Extracellular Mg2+ on Thrombin-Induced and Capacitative Ca2+ Entry in Human Coronary Arterial Endothelial Cells Arterioscler Thromb Vasc Biol, November 1, 1997; 17(11): 3356 - 3361. [Abstract] [Full Text]