Store-operated Ca2+ channels in rat colonic smooth muscle cells.
- Author:
Hua ZHOU
1
;
De-Hu KONG
;
Rong MA
;
Dao-Ping KE
;
Jin-Lan HU
;
Jie SONG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Caffeine; pharmacology; Calcium; metabolism; Calcium Channels; physiology; Colon; cytology; Fura-2; metabolism; Myocytes, Smooth Muscle; drug effects; metabolism; Rats; Rats, Wistar; Thapsigargin; pharmacology
- From: Chinese Journal of Applied Physiology 2006;22(2):220-224
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo study whether store-operated Ca2+ channel (SOC) is present in rat colonic smooth muscle cells.
METHODSIntracellular Ca2+ ([Ca2+]i) changes induced by thapsigargin- or caffeine-activated SOC channel were measured in enzymatically dissociated rat colonic smooth muscle cells with the fluorescent indicator Fura-2/AM.
RESULTSIn the absence of external Ca2+ , the sarco-endoplasmic reticulum Ca2+ pump inhibitor thapsigargin (1 micromol/L) and ryanodine receptor (RyR) activator caffeine both transiently elevated [Ca2+]i from (68.32 +/- 3.43) nmol/L to (240.85 +/- 12.65 ) nmol/L, (481.25 +/- 34.77) nmol/L. A subsequent reintroduction of Ca2+ into the extracellular solution resulted in [Ca2+]i further elevated to (457.55 +/- 19.80) nmol/L, (1005.93 +/- 54.62) nmol/L; (643.88 +/- 34.65) nmol/L, (920.16 +/- 43.25) nmol/L, respectively. And the elevated response was blocked by lanthanum (1 mmol/L), but was insensitive to L-type voltage calcium channels blocker verapamil and membrane depolarization.
CONCLUSIONSOC activated by store depletion are present in rat colonic smooth muscle cells. And we further prove the existence of such Ca2+ channels in excitable cells.