Roles of Ca²⁺ and Na⁺ in the inward current and action potentials of guinea pig ureteral myocytes

Physiological roles of Ca²⁺ vs. Na⁺ in membrane currents and action potentials of ureteral myocytes were investigated on freshly dissociated guinea pig ureteral myocytes with the patch-damp method. The myocytes are spindle shaped, with cell volume of 2,473 μm³, surface area of 2,014 μm², capacitance of 48.2 pF, resting potential of 47.9 mV, and membrane conductance of 840 pS. The membrane current consists of a slow inward Ca²⁺ current (I(Ca)) conducted by L-type Ca²⁺ channels and an actively fluctuating Ca²⁺activated K⁺ current [I(K(Ca))] conducted by Ca²⁺- activated maxi-K⁺ channels. I(Ca) dominates the membrane current by being long lasting and more active at less depolarized potentials than I(K(Ca)) and by regulating I(K(Ca)). Ca²⁺-free media, Co²⁺, and nifedipine reduce or block I(Ca), whereas high extracellular Ca²⁺ concentration and BAY K 8644 enhance it. Action potential amplitudes and plateaus are regulated correspondingly. Related changes are also seen in I(K(Ca)). In contrast, no fast inward current attributable to Na⁺ was found. Replacing extracellular Na⁺ with tris(hydroxymethyl)aminomethane had no apparent effects on the inward or outward current or on the action potentials.