Ca2+ induced inhibition of 45ca influx and ca2+ current in smooth
muscle of the rat vas deferens.
Khoyi, Mohammad A., Tomohisa Ishikawa, Kathleen D. Keef & David P.
Westfall.
Departments of Pharmacology and Physiology, University of Nevada
School of Medicine, Reno, NV 89557-0046, USA
APStracts 2:0427C, 1995.
The present study investigates how changes in [Ca]i modulate the
influx of 45Ca in isolated rat vasa deferentia. Raising [K]o to >/=
32 mM increased 45Ca influx during the first min in solutions
containing 0.03 to 1.5 mM [Ca]o. During the sixth min in [K]o >/= 50
mM, 45Ca influx was less than during the first min. This decline in
45Ca influx occurred for [Ca]o >/= 0.4 mM. Procaine potentiated K+
stimulated 45Ca influx in 1.5 mM [Ca]o and eliminated the decline of
45Ca influx in low [Ca]o. Ryanodine and norepinephrine reduced K+
stimulated 45Ca influx. 45Ca content changed with time in accordance
with the changes observed in 45Ca influx. In isolated cells, voltage
dependent inward currents inactivated more rapidly with 1.5 mM Ca2+
as the charge carrier than with 1.5 mM Ba2+ and the steady state
inactivation relationship was shifted in the hyperpolarizing
direction. Inward current was reduced with either caffeine, ryanodine
or norepinephrine. The inhibitory effects of norepinephrine were
abolished by depletion of intracellular Ca2+ stores. These results
are compatible with the hypothesis that K+ stimulated 45Ca influx
declines with time due to Ca2+-induced inhibition of Ca2+ channels.
Ca2+- and IP3-induced release of Ca2+ from the SR appear to play an
important role in this process.
Received 3 April 1995; accepted in final form 30 October 1995.
APS Manuscript Number C189-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95