TY - JOUR
T1 - Chloride-dependent calcium transients induced by angiotensin II in vascular smooth muscle cells
AU - Ma, Yunn Hwa
AU - Wei, Hsiao Wen
AU - Su, Kwan Hwa
AU - Ives, Harlan E.
AU - Morris, R. Curtis
PY - 2004/1
Y1 - 2004/1
N2 - 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 Ca2+ concentration ([Ca2+]i) is Cl- dependent. After incubating the cells at different extracellular Cl- concentration ([Cl-]e) for 40 min, the ANG II-induced Ca2+ 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 Ca2+, ANG II-induced as well as platelet-derived growth factor-induced Ca2+ release exhibited Cl- dependency. The difference of Ca2+ 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-]c did not affect thapsigargin-induced Ca 2+ release, suggesting that Cl- may not affect the size of intracellular Ca2+ stores. Nevertheless, at high [Cl-], the peak increase of inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] induced by ANG II was approximately sixfold that at low [Cl-]. Thus the Cl--dependent effects of ANG II on Ca2+ transients may be mediated, at least in part, by a Cl--dependent Ins(1,4,5)P3 accumulation in VSMC.
AB - 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 Ca2+ concentration ([Ca2+]i) is Cl- dependent. After incubating the cells at different extracellular Cl- concentration ([Cl-]e) for 40 min, the ANG II-induced Ca2+ 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 Ca2+, ANG II-induced as well as platelet-derived growth factor-induced Ca2+ release exhibited Cl- dependency. The difference of Ca2+ 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-]c did not affect thapsigargin-induced Ca 2+ release, suggesting that Cl- may not affect the size of intracellular Ca2+ stores. Nevertheless, at high [Cl-], the peak increase of inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] induced by ANG II was approximately sixfold that at low [Cl-]. Thus the Cl--dependent effects of ANG II on Ca2+ transients may be mediated, at least in part, by a Cl--dependent Ins(1,4,5)P3 accumulation in VSMC.
KW - Anion
KW - Ca release
KW - Inositol 1,4,5-trisphosphate
UR - http://www.scopus.com/inward/record.url?scp=0346727509&partnerID=8YFLogxK
U2 - 10.1152/ajpcell.00605.2002
DO - 10.1152/ajpcell.00605.2002
M3 - 文章
C2 - 14660489
AN - SCOPUS:0346727509
SN - 0363-6143
VL - 286
SP - C112-C118
JO - American Journal of Physiology - Cell Physiology
JF - American Journal of Physiology - Cell Physiology
IS - 1 55-1
ER -