Ma. Khoyi et al., CA2-INDUCED INHIBITION OF CA-45(2+) INFLUX AND CA2+ CURRENT IN SMOOTH-MUSCLE OF THE RAT VAS-DEFERENS(), American journal of physiology. Cell physiology, 39(5), 1996, pp. 1468-1477
The present study investigates how changes in intracellular Ca2+ conce
ntration modulate the influx of Ca-45(2+) in isolated rat vasa deferen
tia. Raising extracellular K+ concentration ([K+](o)) to greater than
or equal to 32 mM increased Ca-45(2+) influx during the Ist min in sol
utions containing 0.03-1.5 mM extracellular Ca2+ concentration ([Ca2+]
(o)). During the 6th min in [K+](o) greater than or equal to 50 mM, Ca
-45(2+) influx was less than during the 1st min. This decline in Ca-45
(2+) influx occurred for [Ca2+](o) greater than or equal to 0.4 mM. Pr
ocaine potentiated K+-stimulated Ca-45(2+) influx in 1.5 mM [Ca2+](o)
and eliminated the decline of Ca-45(2+) influx in low [Ca2+](o). Ryano
dine and norepinephrine reduced K+-stimulated Ca-45(2+) influx. Ca-45(
2+) content changed with time in accordance with the changes observed
in Ca-45(2+) influx. In isolated cells, voltage-dependent inward curre
nts inactivated more rapidly with 1.5 mM Ca2+ as the charge carrier th
an with 1.5 mM Ba2+, and the steady-state inactivation relationship wa
s shifted in the hyperpolarizing direction. Inward current was reduced
with either caffeine, ryanodine, or norepinephrine. The inhibitory ef
fects of norepinephrine were abolished by depletion of intracellular C
a2+ stores. These results are compatible with the hypothesis that K+-s
timulated Ca-45(2+) influx declines with time due to Ca2+-induced inhi
bition of Ca2+ channels. Ca2+- and inositol 1,4,5-trisphosphate-induce
d releases of Ca2+ from the sarcoplasmic reticulum appear to play an i
mportant role in this process.