PMID- 8877897
OWN - NLM
STAT- MEDLINE
DCOM- 19970123
LR  - 20131121
IS  - 0867-5910 (Print)
IS  - 0867-5910 (Linking)
VI  - 47
IP  - 3
DP  - 1996 Sep
TI  - The source of contracticle calcium in guinea-pig cardiac myocytes treated with 
      thapsigargin.
PG  - 411-23
AB  - We investigated the source of activator Ca2+ in the cells deprived of 
      sarcoplasmic reticulum (SR) Ca2+ by pretreatment with 10(-6) mM thapsigargin 
      (TG). These cells show Ca2+ transients of nearly normal amplitude, albeit with 
      the slowed kinetics. We found in the voltage clamped and loaded with Indo 1-AM 
      cells that at depolarizing potentials from -30 to +70mV, blocking of sarcolemmal 
      Ca2+ channels with 20 microM nifedipine or 20 microM Cd2+ reduced Ca2+ transients 
      and contractions as much in the cells treated with TG as in the normal cells. The 
      residual Ca2+ transients were mostly subthreshold for the contractile system. The 
      result suggests that in the cells treated with TG, Ca2+ influx by the reversed 
      Na/Ca exchange is not more important for activation of contraction than in the 
      normal cells. In the normal cells shortening of one of the depolarizing pulses (+ 
      5mV) applied at a steady rate of 30/min from 200 ms to 5, 10, 20, 30, 50, or 100 
      ms little affected amplitude of the respective Ca2+ transients, although their 
      duration was decreased proportionally to the decrease of the duration of the 
      pulse. In the cells pretreated with TG, 20 ms pulses initiated Ca2+ transients 
      which were hardly visible in the records of fluorescence. Their amplitude 
      increased with increase in the duration of the pulses linearly correlating with 
      the charge transfered with the Ca2+ current. We propose that the direct source of 
      Ca2+ activating contraction in the guinea-pig ventricular myocytes is sarcolemmal 
      Ca2+ influx mostly through the sarcolemmal Ca2+ channels. The alternative 
      hypothesis is that there is some yet unidentified cellular source of activator 
      Ca2+ (internal leaflet of sarcolemma?) from which it may be released by 
      sarcolemmal Ca2+ influx.
FAU - Janiak, R
AU  - Janiak R
AD  - Department of Clinical Physiology, Medical Center of Postgraduate Education, 
      Warsaw, Poland.
FAU - Lewartowski, B
AU  - Lewartowski B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Poland
TA  - J Physiol Pharmacol
JT  - Journal of physiology and pharmacology : an official journal of the Polish 
      Physiological Society
JID - 9114501
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Calcium Channels)
RN  - 67526-95-8 (Thapsigargin)
RN  - I9ZF7L6G2L (Nifedipine)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Calcium/*metabolism
MH  - Calcium Channel Blockers/pharmacology
MH  - Calcium Channels/*metabolism
MH  - Electrophysiology
MH  - Female
MH  - Guinea Pigs
MH  - Heart Ventricles
MH  - Male
MH  - Myocardial Contraction
MH  - Myocardium/cytology/*metabolism
MH  - Nifedipine/metabolism
MH  - Sarcolemma/*metabolism
MH  - Sarcoplasmic Reticulum/*metabolism
MH  - Thapsigargin/*pharmacology
EDAT- 1996/09/01 00:00
MHDA- 1996/09/01 00:01
CRDT- 1996/09/01 00:00
PHST- 1996/09/01 00:00 [pubmed]
PHST- 1996/09/01 00:01 [medline]
PHST- 1996/09/01 00:00 [entrez]
PST - ppublish
SO  - J Physiol Pharmacol. 1996 Sep;47(3):411-23.