Ultra-slow voltage-dependent inactivation of the calcium current in guinea-pig and ferret ventricular myocytes

1994 ◽  
Vol 428 (1) ◽  
pp. 39-50 ◽  
Author(s):  
M. R. Boyett ◽  
H. Honjo ◽  
S. M. Harrison ◽  
W. -J. Zang ◽  
M. S. Kirby
1992 ◽  
Vol 263 (2) ◽  
pp. H410-H417 ◽  
Author(s):  
J. Wu ◽  
P. B. Corr

Long-chain acylcarnitines (LCAC) increase 3.5-fold within 2 min in ischemic myocardium in vivo, and previous studies have suggested, through indirect evidence, that LCAC can stimulate the voltage-dependent L-type Ca2+ current [ICa(L)] in both cardiac and smooth muscle cells. In the present study, whole cell voltage-clamp procedures were performed in isolated adult guinea pig ventricular myocytes to assess the direct effect of LCAC on ICa(L). The intracellular solution contained (in mM) 80 CsCl, 40 K-aspartic acid, and 5 ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). Maximal current density of ICa(L) at 0 mV was 10.1 +/- 0.5 pA/pF (n = 22) at extracellular Ca2+ concentration ([Ca2+]o) = 2.7 mM. LCAC induced a concentration (1-25 microM, n = 23)- and time-dependent, reversible decrease in ICa(L). When delivered extracellularly for 10 min, LCAC (5 microM) inhibited the maximal current of ICa(L) by 48.1 +/- 1.3% (n = 9, P less than 0.01) and shifted the half-maximal voltage of steady-state activation and inactivation from -13.1 +/- 0.5 to -6.8 +/- 0.4 mV (n = 4; P less than 0.05) and from -21.8 +/- 0.2 to -16.5 +/- 0.6 mV (n = 4; P less than 0.01), respectively. Intracellular delivery of LCAC (5 microM) also suppressed ICa(L) to a similar degree (47.5 +/- 1.5%, n = 4; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)


1999 ◽  
Vol 126 (7) ◽  
pp. 1531-1533 ◽  
Author(s):  
George P Thomas ◽  
Morris Karmazyn ◽  
Andrew C Zygmunt ◽  
Charles Antzelevitch ◽  
Njanoor Narayanan

1994 ◽  
Vol 648 (2) ◽  
pp. 296-298 ◽  
Author(s):  
Takehito Yamamoto ◽  
Seiji Kakehata ◽  
Takehisa Saito ◽  
Hitoshi Saito ◽  
Norio Akaike

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