Multiple effects of alpha-adrenoceptor stimulation on the action potential of the rabbit atrium.

Effects of alpha-adrenoceptor stimulation by phenylephrine (10(-7)-10(-4) mol/l) in the presence of pindolol (10(-7) mol/l) on the action potential and force of contraction were observed in the rabbit left atrium. Phenylephrine reduced resting potential, prolonged action potential duration (APD), decreased maximum rate of rise of action potential (Vmax) and increased force of contraction in a concentration-dependent manner. Effects of phenylephrine (10(-5) mol/l) were antagonized by prazosin (10(-7) mol/l) or phentolamine (10(-6) mol/l). APD which had been prolonged by phenylephrine (10(-5) mol/l) was slightly shortened by Ni2+ (0.3 mmol/l) at the level of 50% repolarization but almost unaffected at the level of 90% repolarization. TTX (10(-6) mol/l) had no effect on ADP which had been prolonged by phenylephrine (10(-5) mol/l). Cs+ (10 mmol/l), which inhibits outward current ik1, depolarized resting potential, but in contrast with phenylephrine Cs+ did not affect APD at 90% repolarization. Phenylephrine (10(-5) or 3 X 10(-5) mol/l) restored Ca2+-dependent action potential and force of contraction in 20 mmol/K+-Tyrode solution. These responses were suppressed by prazosin (10(-7) mol/l) or Ni2+ (0.3 mmol/l). Phenylephrine (10(-5) or 10(-4) mol/l) had no effect on steady-state membrane potential--Vmax relationship. It is concluded that in the rabbit left atrium phenylephrine, via alpha-adrenoceptors may suppress outward currents perhaps ik1 and ix, and might increase slow inward current.