Bay K 8644 enhances slow inward and outward currents in voltage-clamped frog skeletal muscle fibres

Cognard, C.; Traoré, F.; Potreau, D.; Raymond, G.

Pflugers Archiv European Journal of Physiology 407(6): 677-683

1986


ISSN/ISBN: 0031-6768
PMID: 2432473
DOI: 10.1007/bf00582651
Accession: 037919191

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Abstract
In isolated frog skeletal muscle fibre slow inward calcium current and slow outward potassium current were recorded by means of a double mannitol-gap device. Bay K 8644, the so-called Ca-channel activator, shifted the activation threshold of the slow inward calcium current (recorded in Cl-free, Ca-rich solution), towards negative potential by 15 mV. It increased the peak current amplitude in a dose-dependent manner (from 10(-11) to 10(-7) M; EC50 approximately equal to 10(-9) M). Apamin, the bee venom toxin which is known to specifically block a class of calcium-dependent potassium channels, failed to block the slow inward calcium current and slowed down its declining phase. This effect exhibited a potential dependence: the more the membrane was depolarized, the more the current decay was slowed down. Bay K 8644 (10(-7) M) transiently decreased the slow outward potassium current, which then progressively increased to stabilize at 135% of the control value. This effect seemed to be more pronounced at potentials above the reversal potential for inward ICa. The results suggest that the increase of the slow outward current is due to a direct action of Bay K 8644 on the slow K channel, rather than an indirect action via potentiation of slow inward calcium current. Moreover, results obtained with apamin indicated that the slow outward potassium current is unlikely to flow through Ca-channels.

Bay K 8644 enhances slow inward and outward currents in voltage-clamped frog skeletal muscle fibres