ICa inactivation was significantly slower in detubulated rat ventricular myocytes compared to control cells (27.1 vs 16.4 ms; P<0.05), indicating t-tubules regulate transsarcolemmal Ca2+ flux.
Absolute Event Rate: 27.1% vs 16.4%
p-value: p=<0.05
We have characterized modulation of ICa by Ca2+ at the t-tubules (ie, in control cells) and surface sarcolemma (ie, in detubulated cells) of cardiac ventricular myocytes, using the whole-cell patch clamp technique to record ICa. ICa inactivation was significantly slower in detubulated cells than in control cells (27.1+/-7.8 ms, n=22, versus 16.4+/-7.9 ms, n=22; P<0.05). In atrial myocytes, which lack t-tubules, ICa inactivation was not changed by the treatment used to produce detubulation. In the presence of ryanodine or BAPTA, or when Ba2+ was used as the charge carrier, the rate of inactivation was not significantly different in control and detubulated cells. Frequency-dependent facilitation occurred in control cells but not in detubulated cells, and was abolished by ryanodine. These results suggest that Ca2+ released from the SR has a greater effect on ICa in the t-tubules than at the surface sarcolemma. This does not appear to be due to differences in local Ca2+ release from the SR, because the gain of Ca2+ release was not significantly different in control and detubulated cells. These data suggest that the t-tubules are a key site for the regulation of transsarcolemmal Ca2+ flux by Ca2+ release from the SR; this could play a role in altered Ca2+ homeostasis in pathological conditions. The full text of this article is available online at http://circres.ahajournals.org.
Brette et al. (Tue,) reported a other. Detubulation vs. Control cells was evaluated on ICa inactivation time (ms) (p=<0.05). ICa inactivation was significantly slower in detubulated rat ventricular myocytes compared to control cells (27.1 vs 16.4 ms; P<0.05), indicating t-tubules regulate transsarcolemmal Ca2+ flux.