In:
American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 286, No. 1 ( 2004-01), p. C112-C118
Abstract:
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 – ]. Thu s 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.
Type of Medium:
Online Resource
ISSN:
0363-6143
,
1522-1563
DOI:
10.1152/ajpcell.00605.2002
Language:
English
Publisher:
American Physiological Society
Publication Date:
2004
detail.hit.zdb_id:
1477334-X
SSG:
12
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