PMID- 16236332
OWN - NLM
STAT- MEDLINE
DCOM- 20060414
LR  - 20131121
IS  - 0024-3205 (Print)
IS  - 0024-3205 (Linking)
VI  - 78
IP  - 14
DP  - 2006 Feb 28
TI  - Evidence for capacitative and non-capacitative Ca2+ entry pathways coexist in A10 
      vascular smooth muscle cells.
PG  - 1558-63
AB  - It is generally thought that receptor-operated Ca2+ entry is related to 
      store-operated or capacitative Ca2+ entry mechanism. Recent evidence suggests 
      that non-capacitative Ca2+ entry pathways are also involved in receptor activated 
      Ca2+ influx in many different kinds of cells. In this study, we studied whether 
      alpha1-adrenoreceptor (alpha1-AR)-activated Ca2+ entry is coupled to both 
      capacitative and non-capacitative pathways in A10 vascular smooth muscle cells by 
      fura-2 fluorescence probe and conventional whole-cell patch clamp techniques. We 
      found that both thapsigargin (TG) and phenylephrine (Phe) induced transient 
      increase in cytoplasmic Ca2+ concentration ([Ca2+]i) in Ca2+-free medium, and 
      subsequent addition of Ca2+ evoked a sustained [Ca2+]i rise. When the membrane 
      potential was held at -60 mV, both TG and Phe activated inward currents, which 
      were inhibited by GdCl3(Gd3+), 0Na+/0Ca2+ solution and 
      1-beta[3-(4-mehtoxyphenyl)propoxy]-4-methoxypheneth-yl-1H- imidazole 
      hydro-chloride (SK&F96365), but not by nifedipine. When Ca2+ store was depleted 
      by TG in Ca2+-free solution, Phe failed to further evoke [Ca2+]i rise. However, 
      when capacitative Ca2+ entry was activated by TG in the medium containing Ca2+, 
      10 microM Phe further increased [Ca2+]i. At the same concentration, TG activated 
      an inward cation current, subsequent addition of Phe also further induced an 
      inward cation current. Furthermore, the amplitudes of [Ca2+]i increase and 
      current density induced by Phe in the presence of TG were less than that induced 
      by Phe alone. Our results suggest that both capacitative and non-capacitative 
      Ca2+ entry pathways are involved in Ca2+ influx induced by activation of 
      alpha1-AR in A10 vascular smooth muscle cells.
FAU - Zhou, Jia-Guo
AU  - Zhou JG
AD  - Department of Pharmacology, Cardiac and Cerebral Vascular Research Center, 
      Zhongshan Medical College, Sun Yat-Sen University 74 Zhongshan 2 Rd Guangzhou, 
      Guangdong, 510089, China.
FAU - Qiu, Qin-Ying
AU  - Qiu QY
FAU - Zhang, Zheng
AU  - Zhang Z
FAU - Liu, Yu-Jie
AU  - Liu YJ
FAU - Guan, Yong-Yuan
AU  - Guan YY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20051017
PL  - Netherlands
TA  - Life Sci
JT  - Life sciences
JID - 0375521
RN  - 0 (Adrenergic alpha-Agonists)
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Calcium Channels)
RN  - 0 (Fluorescent Dyes)
RN  - 0 (TRPC Cation Channels)
RN  - 1WS297W6MV (Phenylephrine)
RN  - 67526-95-8 (Thapsigargin)
RN  - SY7Q814VUP (Calcium)
RN  - TSN3DL106G (Fura-2)
SB  - IM
MH  - Adrenergic alpha-Agonists/pharmacology
MH  - Animals
MH  - Calcium/*metabolism
MH  - Calcium Channel Blockers/pharmacology
MH  - Calcium Channels/drug effects/*metabolism
MH  - Cells, Cultured
MH  - Fluorescent Dyes/analysis
MH  - Fura-2/analysis
MH  - Membrane Potentials/drug effects
MH  - Muscle, Smooth, Vascular/cytology/drug effects/*metabolism
MH  - Myocytes, Smooth Muscle/drug effects/*metabolism
MH  - Patch-Clamp Techniques
MH  - Phenylephrine/pharmacology
MH  - Rats
MH  - TRPC Cation Channels/drug effects/*metabolism
MH  - Thapsigargin/pharmacology
EDAT- 2005/10/21 09:00
MHDA- 2006/04/15 09:00
CRDT- 2005/10/21 09:00
PHST- 2005/06/09 00:00 [received]
PHST- 2005/07/15 00:00 [accepted]
PHST- 2005/10/21 09:00 [pubmed]
PHST- 2006/04/15 09:00 [medline]
PHST- 2005/10/21 09:00 [entrez]
AID - S0024-3205(05)00941-0 [pii]
AID - 10.1016/j.lfs.2005.07.022 [doi]
PST - ppublish
SO  - Life Sci. 2006 Feb 28;78(14):1558-63. doi: 10.1016/j.lfs.2005.07.022. Epub 2005 
      Oct 17.