Low-voltage triggering of Ca[sup 2+] release from the sarcoplasmic reticulum in cardiac muscle cells.

This study in- vestigated the interaction between L-type Ca[sup 2+] current (ICaL) and Ca[sup 2+] release from the sarcoplasmic reticulum (SRCR) in whole cell voltage-clamped guinea pig ventricular myocytes. Quasiphysiological cation solutions (Na[sup +, sub o]:K[sup +, sub I]) were used for most experiments. In control conditions, there was no obvious interaction between ICaL and SRCR. In isoproterenol, activation of ICaL from voltages between -70 and -50 mV reduced the amplitude and accelerated the decay of the current. Short (50 ms), small-amplitude voltage steps applied 60 or 510 ms before stimulating ICaL inhibited and facilitated the current, respectively. These changes were blocked by ryanodine. Low-voltage activated currents such as T-type Ca[sup 2+] current, TTX-sensitive ICa (ICaTTX), or "slip mode" Ca[sup 2+] conductance via INa+ were not responsible for low-voltage SRCR. However, L-type Ca[sup 2+] currents could be distinguished at voltages as negative as -45 mV. It is concluded that in the presence of isoproterenol, Ca[sup 2+] release from the SR at negative potentials is due to activation of L-type Ca[sup 2+] channels. [ABSTRACT FROM AUTHOR]