The roles of ca2+ and na+ in the inward current and action
potentials of guinea pig ureteral myocytes.
Sui, J. L., and C. Y. Kao.
Department of Pharmacology, State University of New York, Health
Science Center at Brooklyn, Brooklyn, New York 11203
APStracts 3:0294C, 1996.
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 patch-clamp method. The
myocytes are spindle shaped, with cell volume of 2473 [mu]m3, surface
area of 2014 [mu]m2, 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 ICa, conducted by L-type Ca2+ channels, and
an actively fluctuating 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 [Ca2+]o 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 had no apparent effects on either the inward or outward
current, or on the action potentials.
Received 22 March 1996; accepted in final form 9 September 1996.
APS Manuscript Number C163-6.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 7 October 1996