Sarcoplasmic reticulum Ca release triggered by Na/Ca exchange is highly temperature sensitive compared to that triggered by Ca current in guinea pig ventricular myocytes.
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Temperature sensitivity of Na/Ca exchange Ca release cautions against room-temperature myocyte data; leaves open its role at physiological temperatures in vivo.
Contractile tension in response to 200-ms voltage-clamp pulses was measured in isolated guinea pig ventricular cells conditioned to constant Ca load. At 23 degrees C, the tension-voltage relation was bell shaped, decaying from a maximum at +20 mV to zero at +100 mV, but at 35 degrees C it was sigmoidal, with similar twitch tensions at +20 and +100 mV. Tension at 35 degrees C and +100 mV was reduced by ryanodine or caffeine and abolished by removal of Ca just before the test pulse. At 35 degrees C and +100 mV, twitch tension increased markedly as the Na concentration in the patch pipette ([Na]p) was varied between 0 and 20 mM. Cd (300 microM) blocked tension at all potentials at 23 degrees C, but tension remained in the presence of Cd at 35 degrees C (29% of control at +2 mV and 100% of control at +100 mV). Cd-resistant tension began to relax during the clamp pulse at all potentials (80 +/- 10 ms at +2 mV and 140 +/- 12 ms at +100 mV). Ni (3.6 mM) both reduced and slowed tension transients at all potentials. The results suggest that fast contractions due to sarcoplasmic reticulum Ca release can be triggered by Ca influx through either Ca current (ICa) or Na/Ca exchange and that those triggered through exchange are much more temperature sensitive than those triggered by ICa.
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Vornanen et al. (1994) studied this question.
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