Adrenaline diminishes K+ contractures and Ba2+-current in chicken slow skeletal muscle fibres

The effects of adrenaline and the β-adrenergic agonist isoprenaline on K+-evoked tension (K+-contracture) and Ba2+ current were investigated in chicken slow (anterior latissimus dorsi (ald)) muscle using isometric-tension measurements and current recording. Addition of adrenaline (10−7–10−5M) or isoprenaline (10−6–10−5 M) to the bath reduced the amplitude of the K+-contractures. These effects were blocked by the β-antagonist propranolol (5 × 10−6 M). External application of a cAMP analogue (8-bromo cyclic AMP; 1 × 10−4 M) also decreased the amplitude of the K+-contractures. To analyze the possible relationship between the induced tension reduction and effects on sarcolemmal Ca2+ channels, a slow action potential and a slow inward membrane current were studied in intact ald chicken muscle fibres. When the ald muscle was immersed in a Na+- and Cl−-free solution containing Ba2+ and depolarizing pulses were delivered from a −80 mV holding potential, the muscle fibres exhibited a small, slow Ba2+-dependent potential (observed at about −26 mV, peak amplitude, around −10 mV). The response was blocked by the addition of Co2+ (5 mM) or Cd2+ (2 mM). Using the three-microelectrode voltage-clamp technique, a slow inward membrane current underlying the Ba2+ potential could be discerned. The current had a mean threshold of −60 mV, reached maximum at about −5 mV and ranged from ca. 9 to 19 μA/cm2 (depending on the external Ba2+ concentration). It had a mean reversal potential of +45 mV. The Ba2+ inward current was diminished when adrenaline or isoprenaline was added to the bath (1 × 10−5 M); however, this decrease did not occur when propranolol was present (5 × 10−6 M). These results suggest that the decreases in the tension of K+-contractures induced by adrenaline and isoprenaline may occur through β-adrenergic effects on sarcolemmal Ca2+ channels in ald chicken slow muscle fibres.