PMID- 14719028
OWN - NLM
STAT- MEDLINE
DCOM- 20040824
LR  - 20191210
IS  - 0008-4212 (Print)
IS  - 0008-4212 (Linking)
VI  - 81
IP  - 12
DP  - 2003 Dec
TI  - Dependence of cyclopiazonic-acid-induced muscle contractures on extracellular 
      Ca2+.
PG  - 1101-9
AB  - Inhibition of Ca2+ uptake by the sarcoplasmic reticulum decreases cytosolic Ca2+ 
      clearance and also triggers Ca2+ influx in response to Ca2+ store depletion. The 
      role of extracellular Ca2+ in the contractures evoked by cyclo-piazonic acid 
      (CPA) and thapsigargin (TG), Ca2+ pump inhibitors, was assessed in mouse 
      diaphragm. At 3-100 microM, CPA elicited a rapid-onset contracture followed by a 
      large elevation of muscle tone, which corresponded temporally to the monophasic 
      slow contracture evoked by TG (1-30 microM). Irrespective of the differences in 
      profiles, contractures were prevented and inhibited by the removal of 
      extracellular Ca2+, but not by nicardipine and SK&F96365, blockers of 
      voltage-gated (L-type) and receptor-operated Ca2+ channels. Mn2+ and Ni2+ 
      preferentially depressed the fast-phase contracture, whereas long-term 
      pretreatment with LY294002, U73122, and 2-aminoethoxydiphenylborance, inhibitors 
      of phosphatidylinositol kinase, phospholipase C, and inositol trisphosphate 
      receptors, suppressed the slow-phase contracture. When contracture was inhibited, 
      the twitch response remained augmented and prolonged by CPA and TG, indicating 
      that the inhibition was not due to malfunction of the contractile apparatus. For 
      preparations incubated in Ca2+-free medium containing CPA, a monophasic fast 
      upstroke of muscle tone developed as extracellular Ca2+ was restored. The results 
      suggest that the bimodal contracture induced by CPA is mediated by the 
      recruitment of distinct Mn2+- and U73122-sensitive Ca2+ entries. The ongoing 
      two-component Ca2+ entries might merge if the muscle preparation was 
      preconditioned with CPA in Ca2+-free medium to deplete cellular Ca2+ stores.
FAU - Hong, S J
AU  - Hong SJ
AD  - Department of Pharmacology, College of Medicine, National Taiwan University, 
      Taipei, Taiwan. sjhong@ha.mc.ntu.edu.tw
FAU - Liang, Hsiu-Chuan
AU  - Liang HC
FAU - Shen, Ching-Jung
AU  - Shen CJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Canada
TA  - Can J Physiol Pharmacol
JT  - Canadian journal of physiology and pharmacology
JID - 0372712
RN  - 0 (Cations, Divalent)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Estrenes)
RN  - 0 (Indoles)
RN  - 0 (Pyrrolidinones)
RN  - 112648-68-7 
      (1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione)
RN  - 42Z2K6ZL8P (Manganese)
RN  - 67526-95-8 (Thapsigargin)
RN  - 7OV03QG267 (Nickel)
RN  - EC 7.2.2.10 (Calcium-Transporting ATPases)
RN  - SY7Q814VUP (Calcium)
RN  - X9TLY4580Z (cyclopiazonic acid)
SB  - IM
MH  - Animals
MH  - Calcium/pharmacology/*physiology
MH  - Calcium-Transporting ATPases/*antagonists & inhibitors/metabolism
MH  - Cations, Divalent
MH  - Diaphragm/*drug effects/innervation/physiology
MH  - Enzyme Inhibitors/pharmacology
MH  - Estrenes/pharmacology
MH  - In Vitro Techniques
MH  - Indoles/antagonists & inhibitors/*pharmacology
MH  - Manganese/pharmacology
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Muscle Contraction/*drug effects/physiology
MH  - Nickel/pharmacology
MH  - Phrenic Nerve/drug effects/physiology
MH  - Pyrrolidinones/pharmacology
MH  - Sarcoplasmic Reticulum/enzymology/physiology
MH  - Thapsigargin/*pharmacology
EDAT- 2004/01/14 05:00
MHDA- 2004/08/25 05:00
CRDT- 2004/01/14 05:00
PHST- 2004/01/14 05:00 [pubmed]
PHST- 2004/08/25 05:00 [medline]
PHST- 2004/01/14 05:00 [entrez]
AID - y03-116 [pii]
AID - 10.1139/y03-116 [doi]
PST - ppublish
SO  - Can J Physiol Pharmacol. 2003 Dec;81(12):1101-9. doi: 10.1139/y03-116.