Modulation of pacemaker activity in sheep cardiac Purkinje fibers by stimulation of ?-adrenoceptor subtypes

1997 ◽  
Vol 92 (1) ◽  
pp. 25-34
Author(s):  
U. Thome ◽  
F. Berger ◽  
U. Borchard ◽  
D. Hafner
1983 ◽  
Vol 244 (1) ◽  
pp. C110-C114 ◽  
Author(s):  
C. O. Lee ◽  
M. Vassalle

The actions of norepinephrine and high calcium on the electrical, mechanical, and intracellular sodium ion activities were studied in electrically driven canine cardiac Purkinje fibers under different conditions. It was found that norepinephrine and high calcium decrease intracellular sodium ion activity (aiNa). The exposure to either agent is followed by a transient decline of force that correlates with the lower aiNa. Inhibition of the Na+ -K+ pump by strophanthidin reduces or abolishes the decrease in aiNa by norepinephrine but not that by high calcium. It is concluded that norepinephrine and high calcium both decrease aiNa and thereby the contractile force but (unlike high calcium) norepinephrine acts through the stimulation of the Na+ -K+ pump.


1978 ◽  
Vol 375 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Pierre-Paul van Bogaert ◽  
Johan S. Vereecke ◽  
Edward E. Carmeliet

1974 ◽  
Vol 64 (3) ◽  
pp. 293-319 ◽  
Author(s):  
Richard W. Tsien

Epinephrine promotes spontaneous activity in cardiac Purkinje fibers through its action on the pacemaker potassium current (iKK2). 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 iKK2 during pacemaker activity by displacing the kinetic parameters of iKK2 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 iKK2, or the underlying inward leakage current, or the threshold for iNNa. The dose dependence of the voltage shift in the iKK2 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 ß-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 ß8, 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 iKK2 channel.


1979 ◽  
Vol 73 (6) ◽  
pp. 819-837 ◽  
Author(s):  
D C Gadsby ◽  
P F Cranefield

Thin canine cardiac Purkinje fibers in a fast flow chamber were exposed to K-free fluid for 15 s to 6 min to initiate "sodium loading," then returned to K-containing fluid to stimulate the sodium pump. The electrophysiological effects of enhanced pump activity may result from extracellular K depletion caused by enhanced cellular uptake of K or from an increase in the current generated as a result of unequal pumped movements of Na and K, or from both. The effects of pump stimulation were therefore studied under three conditions in which lowering the external K concentration ([K]0) causes changes opposite to those expected from an increase in pump current. First, the resting potential of Purkinje fibers may have either a "high" value of a "low" (less negative) value: at the low level of potential, experimental reduction of [K]0 causes depolarization, whereas an increase in pump current should cause hyperpolarization. Second, in regularly stimulated Purkinje fibers, lowering [K]0 prolongs the action potential, whereas an increase in outward pump current should shorten it. Finally, lowering [K]0 enhances spontaneous "pacemaker" activity in Purkinje fibers, whereas an increase in outward pump current should reduce or abolish spontaneous activity. Under all three conditions, we find that the effects of temporary stimulation of the sodium pump are those expected from a transient increase in outward pump current, not those expected from K depletion.


1994 ◽  
Vol 80 (6) ◽  
pp. 1360-1368 ◽  
Author(s):  
David F. Stowe ◽  
Juraj Sprung ◽  
Lawrence A. Turner ◽  
John P. Kampine ◽  
Zeljko J. Bosnjak

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