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The effect of temperature on the rate‐dependent decrease of the rat ventricular calcium current
Author(s) -
McMorn SO,
Harrison SM,
Boyett MR
Publication year - 1998
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.1998.sp004091
Subject(s) - stimulation , chemistry , q10 , biophysics , medicine , calcium , endocrinology , heart rate , biology , anatomy , respiration , blood pressure
We have investigated the effect of temperature upon the rate‐dependent decrease in the L‐type Ca2+ current (iCa) in isolated rat ventricular myocytes. Increasing the rate of stimulation from 0.5 to 3.0 Hz for 30s induced a reversible decrease in iCa which was temperature dependent. Compared to control (0.5 Hz), the first beat at 3 Hz was decreased by 38 +/− 7% at 22 degrees C and by 9 +/− 1% at 37 degrees C (mean +/− S.E.M., n = 5, P < 0.05) and, after 30 s of 3 Hz stimulation, iCa was reduced by a further 26 +/− 4 and 21 +/− 2% at 22 and 37 degrees C, respectively. The magnitude of this secondary decline was not significantly different at the two temperatures (P = 0.29). Corroboratory results were obtained from cell‐attached patches which also illustrated that the rate‐dependent decrease in iCa resulted from a reduction of open channel probability. Paired pulse experiments showed that the greater initial rate‐dependent decrease in iCa at 22 degrees C occurred as a result of slower recovery from fast inactivation processes at 22 than at 37 degrees C. Recovery of the channel from fast inactivation was very temperature sensitive with a Q10 of 5.6. In contrast, the secondary, progressive decrease in iCa, which results from incomplete recovery from ultra‐slow voltage‐dependent inactivation, was similar at the two temperatures and appears to be much less temperature dependent.