Effects of epinephrine on the pacemaker potassium current of cardiac Purkinje fibers.
Effects of epinephrine on the pacemaker potassium current of cardiac Purkinje fibers.
复制标题
肾上腺素对心脏Purkinje纤维的起搏器钾电流的影响。
DOI：
10.1085/jgp.64.3.293
复制
发表时间：
1974-09
影响因子：
3.8
通讯作者：
Tsien, R W
中科院分区：
文献类型：
--
作者：
Tsien, R W
Epinephrine promotes spontaneous activity in cardiac Purkinje fibers through its action on the pacemaker potassium current (i KK2). The mechanism of the acceleratory effect was studied by means of a voltage clamp technique. The results showed that the hormone speeds the deactivation of i KK2 during pacemaker activity by displacing the kinetic parameters of i KK2 toward less negative potentials. This depolarizing voltage shift is the sole explanation of the acceleratory effect since epinephrine did not alter the rectifier properties of i KK2, or the underlying inward leakage current, or the threshold for i NNa. The dose dependence of the voltage shift in the i KK2 activation curve was similar in 1.8 and 5.4 mM [Ca]o. The maximal voltage shift (usually ∼20 mV) was produced by epinephrine concentrations of > 10-6 M. The half-maximal effect was evoked by 60 nM epinephrine, nearly an order of magnitude lower than required for half-maximal effect on the secondary inward current (Carmeliet and Vereecke, 1969). The β-blocker propranolol (10-6 M) prevented the effect of epinephrine (10-7M) but by itself gave no voltage shift. Epinephrine shifted the activation rate coefficient α8 to a greater extent than the deactivation rate coefficient β8, and often steepened the voltage dependence of the steady-state activation curve. These deviations from simple voltage shift behavior were discussed in terms of possible mechanisms of epinephrine's action on the i KK2 channel.
