AJP - Regulatory, Integrative and Comparative Physiology, Vol 249, Issue 4 417-R423, Copyright © 1985 by American Physiological Society
Potentiation of nerve-induced bladder contractions after calcium channel blockade
F. G. Carpenter
The potentiation of nerve-induced bladder contractions (NIC) by
tetraethylammonium chloride (TEA), K+, or carbachol could result from a
greater Ca2+ entry through Ca2+ channels in the muscle or from a greater
release of transmitter by nerve terminals. Contractions of equal magnitude
by the rat urinary bladder in vitro were initiated by carbachol, K+, or
transmural stimulation of urinary bladder motor nerves at 1 Hz.
Contractions elicited by K+ or carbachol were drastically reduced by
verapamil (0.5 microM), but NICs were unaffected. Thus the role of Ca2+
channels in NICs seems uncertain. NICs are potentiated approximately 50% by
K+ (15 mM), carbachol (0.5 microM), or 4-aminopyridine (0.2 mM) and over
twofold by TEA (5 mM). Although verapamil (1-5 microM) reduced NICs in a
dose-dependent relation, potentiation by each compound was the same. Thus
Ca2+ channels probably play no role in potentiation. The resistance of the
bladder to distention reflects its viscoelasticity and is Ca2+ sensitive.
Because viscoelasticity was decreased by verapamil coincident with the
reduction in NICs, both may result from lowered intracellular Ca2+ (Cai2+).
However, because the potentiating compounds failed to restore bladder
viscoelasticity, they probably did not elevate Cai2+. Therefore, in
verapamil-treated preparations potentiation is most probably caused by an
enhancement of transmitter release.
