Kd. Thornbury et al., CHARACTERISTICS OF THE NANC POSTSTIMULUS (REBOUND) CONTRACTION OF THEURINARY-BLADDER NECK MUSCLE IN SHEEP, British Journal of Pharmacology, 116(5), 1995, pp. 2451-2456
1 Strips of muscle from sheep bladder neck were set up for tension rec
ording and subjected to electrical held stimulation (EFS) to stimulate
their intramural nerves. 2 In the presence of atropine (1 mu M) and g
uanethidine (I mu M), the response to 1 Hz EFS was biphasic, character
ized by a relaxation during the stimulus period, followed by a post-st
imulus contraction. A similar biphasic response was also seen followin
g bolus application of nitric oxide (NO). 3 In the absence of atropine
and guanethidine, the relaxations were masked by contractions during
stimulation; however, the post-stimulus contractions were unaffected.
L-NAME (100 mu M) blocked the post-stimulus contractions and L-arginin
e (1 mM) restored them, suggesting that they were NO-mediated. 4 M&B 2
2948, a phosphodiesterase inhibitor, prolonged the relaxations and abo
lished the post-stimulus contractions. This suggests that rapid remova
l of cyclic GMP is required for post-stimulus contraction to occur. 5
When the number of pulses in the stimulus train was kept constant, the
size of the post-stimulus contraction increased as the duration of th
e preceding period of stimulation increased. Maximal poststimulus cont
ractions were obtained following stimulation for >40 s. 6 The L-channe
l antagonist, nifedipine (1 mu M) and verapamil(1 mu M), had little ef
fect on the amplitude of the post-stimulus contractions. 7 In contrast
, ryanodine (8 mu M) reduced the post-stimulus contractions by over 90
%. Caffeine (20 mM) also abolished the post-stimulus contractions and
cyclopiazonic acid (CPA, IO mu M) reduced them by 76%. However, in the
presence of CPA a slower post-stimulus contraction developed. Nifedip
ine (1 mu M) reduced this by 40%. 8 In conclusion, these results suppo
rt a role for NO in the post-stimulus contraction of the sheep bladder
neck muscle. The post-stimulus contraction depends more on release of
intracellular Ca2+, than Ca2+ influx through L-type channels.