Document Detail


Nicardipine-sensitive Na+-mediated single channel currents in guinea-pig sinoatrial node pacemaker cells.
MedLine Citation:
PMID:  10562335     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
1. The Na+-dependent inward currents underlying slow diastolic depolarization of sinoatrial (SA) node cells were examined. Using a Na+-rich, Ca2+-free pipette solution a novel single channel current was recorded in addition to the conventional Na+ and L-type Ca2+ currents. The current (termed ist, as it reflects the whole-cell sustained inward current, Ist) does not show obvious inactivation during a 700 ms depolarization and is unique in having a smaller amplitude (1.1 +/- 0.18 pA at -60 mV, n = 12) than the Na+ current through conventional Na+ ( approximately 3.3 pA) and Ca2+ channels (9.6 +/- 0.32 pA at -60 mV, n = 8). The mean unitary conductance of ist channels was 13.3 pS. 2. The recording of ist was infrequent, was observed only in spontaneously beating SA node cells, and was facilitated by adding Bay-K 8644 to the pipette solution. Overlapping of ist events was observed and ist was abolished by bath application of nicardipine. 3. In the ensemble average, the activation of ist was evident by depolarization beyond -70 mV, and the dynamic voltage range of activation (-70 to -30 mV) encompassed the extent of the slow diastolic depolarization. The current density of ist was 0.33 pA pF-1 at -60 mV, as estimated from the number of channels per membrane patch, the open probability and the unitary amplitude. 4. Cumulative histograms for both open and closed times were fitted with a sum of two exponential components. The slow time constants decreased with depolarization, while the fast time constants and the fraction of the fast component were voltage independent. The number of bursts per sweep increased with depolarization. The time constant of the first latency histogram was about two orders of magnitude larger than those in cardiac L-type Ca2+ channels and decreased with depolarization. 5. It is suggested that the ist channels might be responsible for the whole-cell Ist.
Authors:
T Mitsuiye; J Guo; A Noma
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Publication Detail:
Type:  Comparative Study; In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of physiology     Volume:  521 Pt 1     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  1999 Nov 
Date Detail:
Created Date:  2000-02-14     Completed Date:  2000-02-14     Revised Date:  2013-06-11    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  69-79     Citation Subset:  IM    
Affiliation:
Department of Physiology, Faculty of Medicine, Kyoto University, Sakyo-ku, Yoshida-Konoe, Kyoto 606-8501, Japan. tamo3@card.med.kyoto-u.ac.jp
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MeSH Terms
Descriptor/Qualifier:
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / pharmacology
Animals
Calcium Channel Agonists / pharmacology
Calcium Channel Blockers / pharmacology*
Calcium Channels, L-Type / drug effects,  metabolism
Guinea Pigs
Ion Channels / drug effects*,  metabolism*
Kinetics
Membrane Potentials
Nicardipine / pharmacology*
Patch-Clamp Techniques
Sinoatrial Node / cytology,  drug effects*,  metabolism*
Sodium / metabolism*
Chemical
Reg. No./Substance:
0/Calcium Channel Agonists; 0/Calcium Channel Blockers; 0/Calcium Channels, L-Type; 0/Ion Channels; 55985-32-5/Nicardipine; 71145-03-4/3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; 7440-23-5/Sodium
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