The role of calcium in modulating the reactivity of the smooth muscle cells during ischemia/reperfusion. Part 1

被引:0
作者
Szadujkis-Szadurska, Katarzyna [1 ]
Szadujkis-Szadurski, Rafal [1 ]
Szadujkis-Szadurski, Leszek [1 ]
Grzesk, Grzegorz [1 ]
Slupski, Maciej [1 ]
Matusiak, Grzegorz [1 ]
Gajdus, Marta [1 ]
Glaza, Izabela [1 ]
机构
[1] Coll Med Bydgoszcz, Pharmacol & Therapy Dept, Bydgoszcz 85094, Czech Republic
来源
POSTEPY HIGIENY I MEDYCYNY DOSWIADCZALNEJ | 2010年 / 64卷
关键词
angiotensin II; phenylephrine; ischemia; reperfusion; calcium; G protein; ANGIOTENSIN-II; NITRIC-OXIDE; INJURY; CA2+; ISCHEMIA; SLEEP;
D O I
暂无
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background: Calcium ions regulate the function of cells in many ways, acting as first messengers of intercellular information and second messengers of intracellular information. Changes in cytoplasmic calcium levels depend on calcium influx from the extracellular space or calcium release from cellular stores. Increase in calcium ion concentration takes place in pathological situations, such as ischemia. In the present study the roles of calcium and G protein in contraction induced by angiotensin II (agonist of the metabotropic receptor AT1), phenylephrine (agonist of alpha1-adrenergic metabotropic receptor), and Bay K8644 (a calcium channel agonist) after ischemia/reperfusion were investigated. Material/Methods: Experiments were performed on perfused male Wistar rats' tail arteries. Contraction induced by angiotensin II, phenylephrine, and Bay K8644 mediated by intracellular or extracellular calcium after ischemia/reperfusion and in the presence of the blocker of G protein Bordetella pertussis toxin (P 7208) was analyzed. Results: Ischemia reduced while reperfusion augmented the response of vascular smooth muscle cells to angiotensin II and phenylephrine, but they did not change the effects of Bay K8644. P 7208 decreased the effects of phenylephrine mediated by intracellular and extracellular calcium and reduced the reactions of angiotensin II mediated only by intracellular calcium, but did not change the effects of Bay K8644. Conclusions: Ischemia/reperfusion modulates vascular contraction induced by angiotensin II and phenylephrine. Both intracellular and extracellular calcium ions mediate the contraction induced by angiotensin II and phenylephrine. The results suggests that G protein modulates the effects of angiotensin II mediated by intracellular calcium ions while it plays a role in the reactions of phenylephrine mediated by calcium coming from both sources, intracellular and extracellular.
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页码:188 / 194
页数:7
相关论文
共 29 条
[1]   G protein-coupled receptor oligomerization - Implications for G protein activation and cell signaling [J].
Breitwieser, GE .
CIRCULATION RESEARCH, 2004, 94 (01) :17-27
[3]  
de Gasparo M, 2000, PHARMACOL REV, V52, P415
[4]   Trafficking of G protein-coupled receptors [J].
Drake, Matthew T. ;
Shenoy, Sudha K. ;
Lefkowitz, Robert J. .
CIRCULATION RESEARCH, 2006, 99 (06) :570-582
[5]   Excitotoxic death of a subset of embryonic rat motor neurons in vitro [J].
Fryer, HJL ;
Knox, RJ ;
Strittmatter, SM ;
Kalb, RG .
JOURNAL OF NEUROCHEMISTRY, 1999, 72 (02) :500-513
[6]   β-adrenergic stimulation of L-type Ca2+ channels in cardiac myocytes requires the distal carboxyl terminus of α1C but not serine 1928 [J].
Ganesan, AN ;
Maack, C ;
Johns, DC ;
Sidor, A ;
O'Rourke, B .
CIRCULATION RESEARCH, 2006, 98 (02) :E11-E18
[7]   Effect of NO donors on protein phosphorylation in intact vascular and nonvascular smooth muscles [J].
Hennan, JK ;
Diamond, J .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2001, 280 (04) :H1565-H1580
[8]   Update in sleep and control of ventilation 2006 [J].
Horner, Richard L. ;
Bradley, T. Douglas .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2007, 175 (05) :426-431
[9]   Calcium influx through receptor-operated channel induces mitochondria-triggered paraptotic cell death [J].
Jambrina, E ;
Alonso, R ;
Alcalde, M ;
Rodríguez, MD ;
Serrano, A ;
Martínez-A, C ;
García-Sancho, J ;
Izquierdo, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (16) :14134-14145
[10]  
Ji JZ, 1998, J PHARMACOL EXP THER, V285, P16