Differential modulation of caffeine- and IP3-induced calcium release in cultured arterial tissue

被引:13
作者
Dreja, K [1 ]
Hellstrand, P [1 ]
机构
[1] Lund Univ, Dept Physiol Sci, S-22362 Lund, Sweden
来源
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 1999年 / 276卷 / 05期
关键词
sarcoplasmic reticulum; organ culture; tail artery; D-myo-inositol 1,4,5-trisphosphate;
D O I
10.1152/ajpcell.1999.276.5.C1115
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
To investigate the Ca2+-dependent plasticity of sarcoplasmic reticulum (SR) function in vascular smooth muscle, transient responses to agents releasing intracellular Ca2+ by either ryanodine (caffeine) or D-myo-inositol 1,4,5-trisphosphate [IP3; produced in response to norepinephrine (NE), 5-hydroxytryptamine (5-HT), arginine vasopressin (AVP)] receptors in rat tail arterial rings were evaluated after 4 days of organ culture. Force transients induced by all agents were increased compared with those induced in fresh rings. Stimulation by 10% FCS during culture further potentiated the force and Ca2+ responses to caffeine (20 mM) but not to NE (10 mu M), 5-HT (10 mu M), or AVP (0.1 mu M) The effect was persistent, and SR capacity was not altered after reversible depletion of stores with cyclopiazonic acid. The effects of serum could be mimicked by culture in depolarizing medium (30 mM K+) and blocked by the addition of verapamil (1 mu M) or EGTA (1 mM) to the medium, lowering intracellular Ca2+ concentration ([Ca2+](i)) during culture. These results show that modulation of SR function can occur in vitro by a mechanism dependent on long-term levels of basal [Ca2+](i) and involving ryanodine- but not IP3 receptor-mediated Ca2+ release.
引用
收藏
页码:C1115 / C1120
页数:6
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