In guinea pig ureteral myocytes, IKCa plays a key role in maintaining resting potential and repolarizing action potentials, whereas ITO has minimal effects.
IKCa may modulate ureteral myocyte excitability in guinea pigs; leaves open translational relevance to human smooth muscle disorders.
Outward currents of freshly dissociated ureteral myocytes consist mainly of Ca(2+)-activated K+ current (IKCa) and a transient outward current (ITO). No delayed rectifier current was apparent. IKCa is small and nondecaying and fluctuates actively and irregularly. Blocking IKCa decreased resting membrane conductance and prolonged action potential plateaus, showing its roles in maintaining the resting potential and in repolarizing action potentials. It is also responsible for the membrane potential fluctuations on action potential plateaus. Neither 8-(diethylamino)octyl-3,4,5-trimethoxybenzoate hydrochloride nor caffeine reduced the fluctuations in the outward current or in the action potentials, indicating that internal Ca2+ storage contributes little to the fluctuations. ITO has fast activation and inactivation kinetics with inactivation time constants of approximately 15 and 150 ms, respectively. Its highly negative voltage-availability relationship (V0.5 = -70.5 mV) suggests a low availability (< 5%) at normal resting potentials. It has only trivial effects on action potentials.
No takes yet. Share an insight, caveat, or question.
Sui et al. (1997) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: