Regulation of urinary bladder smooth muscle contractions by ryanodine receptors and BK and SK channels

被引:152
作者
Herrera, GM [1 ]
Heppner, TJ
Nelson, MT
机构
[1] Univ Vermont, Coll Med, Dept Mol Physiol & Biophys, Burlington, VT 05405 USA
[2] Univ Vermont, Coll Med, Dept Pharmacol, Burlington, VT 05405 USA
关键词
guinea pig; incontinence; calcium channel; iberiotoxin; apamin; sarcoplasmic reticulum;
D O I
10.1152/ajpregu.2000.279.1.R60
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
This study examines the roles of voltage-dependent Ca2+ channels (VDCC), ryanodine receptors (RyRs), large-conductance Ca2+-activated K+ (BK) channels, and small-conductance Ca2+-activated K+ (SK) channels in the regulation of phasic contractions of guinea pig urinary bladder smooth muscle (UBSM). Nisoldipine (100 nM), a dihydropyridine inhibitor of VDCC, abolished spontaneous UBSM contractions. Ryanodine (10 mu M) increased contraction frequency and thereby integrated force and, in the presence of the SK blocker apamin, had a greater effect on integrated force than ryanodine alone. Blocking BK (iberiotoxin, 100 nM) or SK (apamin, 100 nM) channels increased contraction amplitude and duration but decreased frequency. The contractile response to iberiotoxin was more pronounced than to apamin. The increases in contraction amplitude and duration to apamin were substantially augmented with ryanodine pretreatment. These results indicate that BK and SK channels have prominent roles as negative feedback elements to limit UBSM contraction amplitude and duration. RyRs also appear to play a significant role as a negative feedback regulator of contraction frequency and duration, and this role is influenced by the activity of SK channels.
引用
收藏
页码:R60 / R68
页数:9
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