Egger, Marcel

Niggli, Ernst

Pignier, Christophe

Szentesi, Péter

Pflügers Archiv - European Journal of Physiology

University of Debrecen Electronic Archive

Refractoriness of SR-Calcium Release after betaadrenergic Stimulation in Cardiac 
Myocytes 
 
M Egger, C Pignier, P Szentesi, E Niggli 
Physiologisches Institut, Universität Bern 
 
Some mechanisms of the Ca2+-induced Ca2+ release (CICR) are still a matter of debate, such as 
regulation of CICR. We have observed that in cardiac myocytes coherent activation of SR Ca2+ 
release induced refractoriness of CICR. It has been suggested that SR Ca2+ depletion and 
refilling may underlie refractoriness. Here we examined whether β-adrenergic stimulation could 
affect CICR. We used UV-laser flash photolysis of caged Ca2+ in combination with the whole-
cell patch clamp technique to activate Na+-Ca2+ exchange currents in guinea pig ventricular 
myocytes. Pairs of UV-flashes were applied at various intervals to follow the time-course of 
recovery from refractoriness. β-adrenoreceptor stimulation affected SR Ca2+ content in two 
different ways. (1) Whereas the SR Ca2+ content was decreased when isoproterenol (Iso) 
treatment began after SR reloading, it was elevated if SR reloading was performed during Iso 
superfusion. (2) β-adrenergic stimulation (after SR reloading) resulted in a faster recovery of 
CICR from refractoriness. SR Ca2+ content and RyR phospho-rylation both could lead to 
changes in Ca2+ sensitivity of CICR. Application of 1µM Iso reduced the refractoriness, such 
that complete recovery of Ca2+ release could be observed earlier. We conclude that β-adrenergic 
stimulation may modulate global CICR refractoriness. This might result from acceleration of 
SR Ca2+ refilling or from a change of the Ca2+ sensitivity and/or gating kinetics of the RyRs. 


Refractoriness of SR-Calcium release after betaadrenergic stimulation in cardiac myocytes

https://dea.lib.unideb.hu/dea/bitstream/handle/2437/222346/abstract.pdf?sequence=4&isAllowed=y

Refractoriness of SR-Calcium release after betaadrenergic stimulation in cardiac myocytes

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