PMID- 9884025
OWN - NLM
STAT- MEDLINE
DCOM- 19990323
LR  - 20191210
IS  - 0898-6568 (Print)
IS  - 0898-6568 (Linking)
VI  - 10
IP  - 10
DP  - 1998 Nov
TI  - Dissociation of intracellular Ca2+ release and Ca2+ entry response to 
      5-hydroxytryptamine in cultured canine tracheal smooth muscle cells.
PG  - 735-42
AB  - The relationship between the agonist-sensitive Ca2+ pool and those discharged by 
      the Ca2+ -ATPase inhibitor thapsigargin (TG) were investigated in canine tracheal 
      smooth muscle cells (TSMCs). In fura-2-loaded TSMCs, 5-hydroxytryptamine (5-HT) 
      stimulated a rapid increase in intracellular Ca2+ ([Ca2+]i), followed by a 
      sustained plateau phase that was dependent on extracellular Ca2+. In such cells, 
      TG produced a concentration-dependent increase in [Ca2+]i, which remained 
      elevated over basal level for several minutes and was substantially attenuated in 
      the absence of extracellular Ca2+. Application of 5-HT after TG demonstrated that 
      the TG-sensitive compartment partly overlapped the 5-HT-sensitive stores. 
      Pre-treatment of TSMCs with TG significantly inhibited the increase in [Ca2+]i 
      induced by 5-HT in a time-dependent manner. Similar results were obtained with 
      two other Ca2+ -ATPase inhibitors, cyclopiazonic acid and 
      2,5-di-t-butylhydroquinone. Although these inhibitors had no effect on 
      phosphoinositide hydrolysis, Ca2+ -influx was stimulated by these agents. These 
      results suggest that depletion of the agonist-sensitive Ca2+ stores is sufficient 
      for activation of Ca2+ influx. Some characteristics of the Ca2+ -influx activated 
      by depletion of internal Ca2+ stores were compared with those of the 
      agonist-activated pathway. 5-HT-stimulated Ca2+ influx was inhibited by La3+, 
      membrane depolarisation, and the novel Ca2+ -influx blocker 
      1- inverted question markbeta-[3-(4-methoxyphenyl) propoxy]-4-methoxyphenethyl inverted question mark-1H-imidazole 
      hydrochloride (SKF96365). Likewise, activation of Ca2+ influx by TG also was 
      blocked by La3+, membrane depolarisation, and SKF96365. These results suggest 
      that (1) in the absence of PI hydrolysis, depletion of the agonist-sensitive 
      internal Ca2+ stores in TSMCs is sufficient for activation of Ca2+ influx, and 
      (2) the agonist-activated Ca2+ influx pathway and the influx pathway activated by 
      depletion of the inositol 1,4,5-trisphosphate-sensitive Ca2+ pool are 
      indistinguishable.
FAU - Yang, C M
AU  - Yang CM
AD  - Department of Pharmacology, College of Medicine, Chang Gung University, Tao-Yuan, 
      Taiwan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Cell Signal
JT  - Cellular signalling
JID - 8904683
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Imidazoles)
RN  - 0 (Indoles)
RN  - 0 (Inositol Phosphates)
RN  - 333DO1RDJY (Serotonin)
RN  - 67526-95-8 (Thapsigargin)
RN  - 6I3K30563S (Lanthanum)
RN  - EC 7.2.2.10 (Calcium-Transporting ATPases)
RN  - I61V87164A (1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole)
RN  - SY7Q814VUP (Calcium)
RN  - X9TLY4580Z (cyclopiazonic acid)
SB  - IM
MH  - Animals
MH  - Calcium/*metabolism
MH  - Calcium Channel Blockers/pharmacology
MH  - Calcium-Transporting ATPases/antagonists & inhibitors
MH  - Cells, Cultured
MH  - Dogs
MH  - Enzyme Inhibitors/pharmacology
MH  - Imidazoles/pharmacology
MH  - Indoles/pharmacology
MH  - Inositol Phosphates/*metabolism
MH  - Kinetics
MH  - Lanthanum/pharmacology
MH  - Membrane Potentials/drug effects/physiology
MH  - Muscle, Smooth/drug effects/*physiology
MH  - Serotonin/*pharmacology
MH  - Signal Transduction
MH  - Thapsigargin/pharmacology
MH  - Trachea/drug effects/*physiology
EDAT- 1999/01/12 00:00
MHDA- 1999/01/12 00:01
CRDT- 1999/01/12 00:00
PHST- 1999/01/12 00:00 [pubmed]
PHST- 1999/01/12 00:01 [medline]
PHST- 1999/01/12 00:00 [entrez]
AID - S0898-6568(98)00020-5 [pii]
AID - 10.1016/s0898-6568(98)00020-5 [doi]
PST - ppublish
SO  - Cell Signal. 1998 Nov;10(10):735-42. doi: 10.1016/s0898-6568(98)00020-5.