| pubmed-article:9124296 | pubmed:abstractText | 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-clamp method. The myocytes are spindle shaped, with cell volume of 2,473 microm3, surface area of 2,014 microm2, 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 (ICa) conducted by L-type Ca2+ channels and an actively fluctuating Ca2+-activated K+ current [IK(Ca)] conducted by Ca2+-activated maxi-K+ channels. ICa dominates the membrane current by being long lasting and more active at less depolarized potentials than IK(Ca) and by regulating IK(Ca). Ca2+-free media, Co2+, and nifedipine reduce or block ICa, 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 IK(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. | lld:pubmed |
