M. Kawai et al., Excitation-contraction coupling in rat ventricular myocytes after formamide-induced detubulation, AM J P-HEAR, 46(2), 1999, pp. H603-H609
Citations number
28
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Formamide-induced osmotic shock has been used to detubulate isolated adult
rat ventricular myocytes (i.e., disrupt the surface membrane-T tubule junct
ion). Cell volume, calculated from cell length and width, rapidly decreased
and increased upon application and removal of formamide, respectively. Aft
er treatment with formamide, membrane capacitance decreased by 26.4% (from
199.4 +/- 18.7 pF in control cells to 146.7 +/- 6.4 pF in formamide-treated
cells; n = 1.3, P < 0.05). However, the amplitude of the L-type Ca2+ curre
nt (Ic,) decreased by a greater extent (from 0.75 +/- 0.14 to 0.18 +/- 0.03
nA; n = 5, P < 0.05) so that the density of I-Ca decreased by 74.5%. Simul
taneous measurements of I-Ca and Ca2+ transients (monitored using fura 2) s
howed that both decreased rapidly upon removal of formamide. However, the C
a2+ content of the sarcoplasmic reticulum showed little change. Cross-stria
tions, visualized with the fluorescent dye di-8-aminonaphthylethenylpyridin
ium, were sparse or absent in cells that had been treated with formamide, s
uggesting that formamide can successfully detubulate cardiac cells and that
I-Ca is concentrated in the T tubules, which therefore play an important r
ole in excitation-contraction coupling.