PMID- 9049175
OWN - NLM
STAT- MEDLINE
DCOM- 19970610
LR  - 20190726
IS  - 0031-6768 (Print)
IS  - 0031-6768 (Linking)
VI  - 433
IP  - 6
DP  - 1997 Apr
TI  - Voltage dependence of the Fura-2 transient in rabbit left atrial myocytes at 37 
      degrees C.
PG  - 817-26
AB  - We used the whole-cell patch-clamp technique and monitoring of Fura-2 
      fluorescence to investigate the voltage dependence of the L-type Ca current 
      (ICa,L) and intracellular Ca (Cai) transient in rabbit atrial myocytes at 37 
      degrees C. Imaging the atrial cell membrane with Di-4-ANNEPS showed (in contrast 
      to ventricular cells) that atrial cells had very few transverse tubules. We 
      measured ICa,L using a Cs-based internal dialysis solution to eliminate 
      interfering K currents. The voltage dependence of peak ICa,L amplitude was 
      bell-shaped: ICa,L was maximal at +10 mV and declined at more negative and 
      positive potentials. For measuring the Fura-2 (Cai) transient, we used a K-based 
      internal dialysis solution to preserve normal excitation-contraction coupling. 
      Ryanodine (20 microM) plus thapsigargin (2 microM) (blockers of the sarcoplasmic 
      reticulum, SR) abolished the phasic component of the Fura-2 transient (n = 5), 
      demonstrating that the phasic Fura-2 transient provided an index of the magnitude 
      of SR release. The Fura-2 transient also showed bell-shaped voltage dependence, 
      but this was different from that for ICa,L. The Fura-2 transient peaked at +30 mV 
      and partially declined at more positive potentials; but at potentials where 
      inward ICa,L was small (if not absent), the phasic Fura-2 transient still 
      attained a significant amplitude. We used a rapid application of nifedipine (32 
      microM), and of nifedipine plus 5 mM Ni, to assess the ability of ICa,L and 
      reverse-mode Na-Ca exchange to trigger SR Ca release. With test pulses to +10 mV 
      and +60 mV, a rapid switch to nifedipine (which blocked ICa,L) produced no 
      significant reduction in phasic Fura-2 transient amplitude. This suggests that in 
      the absence of ICa,L, another mechanism was able to trigger SR release. With 
      pulses to +10 and +60 mV, a single beat switch to nifedipine plus 5 mM Ni almost 
      completely abolished the phasic transient. Since 5 mM Ni inhibits Na-Ca exchange, 
      this suggests that, in the absence of ICa,L, trigger Ca entry via reverse Na-Ca 
      exchange was able to activate SR Ca release in atrial cells at 37 degrees C. The 
      mechanisms underlying the Fura-2 transient in atrial cells, and differences with 
      pre-existing data from rabbit ventricular cells, are discussed.
FAU - Mitcheson, J S
AU  - Mitcheson JS
AD  - Department of Physiology University of Bristol, School of Medical Sciences, UK.
FAU - Hancox, J C
AU  - Hancox JC
FAU - Levi, A J
AU  - Levi AJ
LA  - eng
GR  - Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Pflugers Arch
JT  - Pflugers Archiv : European journal of physiology
JID - 0154720
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Carrier Proteins)
RN  - 0 (Fluorescent Dyes)
RN  - 0 (Sodium-Calcium Exchanger)
RN  - 9NEZ333N27 (Sodium)
RN  - SY7Q814VUP (Calcium)
RN  - TSN3DL106G (Fura-2)
SB  - IM
MH  - Animals
MH  - Calcium/*metabolism
MH  - Calcium Channel Blockers/pharmacology
MH  - Carrier Proteins/metabolism
MH  - Electric Stimulation
MH  - Electrophysiology
MH  - Fluorescent Dyes
MH  - Fura-2
MH  - Heart/drug effects
MH  - In Vitro Techniques
MH  - Male
MH  - Membrane Potentials/drug effects/physiology
MH  - Microscopy, Confocal
MH  - Myocardium/cytology/*metabolism
MH  - Patch-Clamp Techniques
MH  - Rabbits
MH  - Sodium/metabolism
MH  - Sodium-Calcium Exchanger
EDAT- 1997/04/01 00:00
MHDA- 1997/04/01 00:01
CRDT- 1997/04/01 00:00
PHST- 1997/04/01 00:00 [pubmed]
PHST- 1997/04/01 00:01 [medline]
PHST- 1997/04/01 00:00 [entrez]
AID - 10.1007/s004240050350 [doi]
PST - ppublish
SO  - Pflugers Arch. 1997 Apr;433(6):817-26. doi: 10.1007/s004240050350.