Chloride-dependent calcium transients induced by angiotensin II in vascular smooth muscle cells

• Published in: American Journal of Physiology: Cell Physiology Vol. 286; no. 1; pp. C112 - C118
• Main Authors: Ma, Yunn-Hwa, Wei, Hsiao-Wen, Su, Kwan-Hwa, Ives, Harlan E, Morris, R. Curtis, Jr
• Format: Journal Article
• Language: English
• Published: United States 01.01.2004
• Subjects: Angiotensin II - pharmacology; Animals; Calcium - metabolism; Chlorides - metabolism; Chlorides - pharmacology; Extracellular Fluid - metabolism; Humans; Intracellular Membranes - metabolism; Male; Muscle, Smooth, Vascular - drug effects; Muscle, Smooth, Vascular - metabolism; Myocytes, Smooth Muscle - drug effects; Myocytes, Smooth Muscle - metabolism; Osmolar Concentration; Rats; Rats, Inbred SHR; Rats, Sprague-Dawley; Vasoconstrictor Agents - pharmacology
• ISSN: 0363-6143; 1522-1563
• DOI: 10.1152/ajpcell.00605.2002

1 Department of Physiology and Pharmacology, College of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan 333, Taiwan, Republic of China; and 2 Department of Medicine, University of California, San Francisco, California 94143 Submitted 7 May 2002 ; accepted in final form 8 September 2003 Cl – is essential for the vasoconstrictive response to angiotensin II (ANG II). In vascular smooth muscle cells (VSMC), we determined whether ANG II-induced transient increase in intracellular Ca 2+ concentration ([Ca 2+ ] i ) is Cl – dependent. After incubating the cells at different extracellular Cl – concentration ([Cl – ] e ) for 40 min, the ANG II-induced Ca 2+ transients at 120 meq/l Cl – were more than twice those at either 80 or 20 meq/l Cl – . Replacing Cl – with bicarbonate or gluconate yielded similar results. In addition, after removal of extracellular Ca 2+ , ANG II-induced as well as platelet-derived growth factor-induced Ca 2+ release exhibited Cl – dependency. The difference of Ca 2+ release with high vs. low [Cl – ] e was not affected by acutely altering [Cl – ] e 1 min before administration of ANG II when [Cl – ] i was yet to be equilibrated with [Cl – ] e . Pretreatment of a Cl – channel inhibitor, 5-nitro-2-(3-phenylpropylamino)benzoic acid, increased ANG II-induced Ca 2+ release and entry at 20 meq/l Cl – but did not alter those at 120 meq/l Cl – . However, after equilibration, a reduced [Cl – ] e did not affect thapsigargin-induced Ca 2+ release, suggesting that Cl – may not affect the size of intracellular Ca 2+ stores. Nevertheless, at high [Cl – ], the peak increase of inositol 1,4,5-trisphosphate [Ins(1,4,5)P 3 ] induced by ANG II was approximately sixfold that at low [Cl – ]. Thus the Cl – -dependent effects of ANG II on Ca 2+ transients may be mediated, at least in part, by a Cl – -dependent Ins(1,4,5)P 3 accumulation in VSMC. anion; inositol 1,4,5-trisphosphate; Ca 2+ release Address for reprint requests and other correspondence: Y.-H. Ma, Dept. of Physiology and Pharmacology, College of Medicine, Chang Gung Univ., 259 Wen-Hwa 1st Road, Kwei-Shan, Tao-Yuan 333, Taiwan (E-mail: yhma{at}mail.cgu.edu.tw ).