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相似文献

1
ATP and other adenine compounds increase mechanical activity and inositol trisphosphate production in rat heart.三磷酸腺苷(ATP)和其他腺嘌呤化合物可增强大鼠心脏的机械活动并增加三磷酸肌醇的生成。
J Physiol. 1988 Jul;401:185-99. doi: 10.1113/jphysiol.1988.sp017157.
2
Purinoceptors in the rat heart.大鼠心脏中的嘌呤受体。
Br J Pharmacol. 1987 Jan;90(1):219-27. doi: 10.1111/j.1476-5381.1987.tb16843.x.
3
The effect of adenyl compounds on the rat heart.腺苷化合物对大鼠心脏的影响。
Br J Pharmacol. 1983 May;79(1):211-8. doi: 10.1111/j.1476-5381.1983.tb10514.x.
4
Distribution of P1- and P2-purinoceptors in the guinea-pig and frog heart.豚鼠和蛙心脏中P1和P2嘌呤受体的分布
Br J Pharmacol. 1981 Aug;73(4):879-85. doi: 10.1111/j.1476-5381.1981.tb08741.x.
5
Stimulation by ATP of inositol trisphosphate accumulation and calcium mobilization in cultured adrenal chromaffin cells.三磷酸腺苷对培养的肾上腺嗜铬细胞中肌醇三磷酸积累和钙动员的刺激作用。
J Neurochem. 1989 Feb;52(2):441-7. doi: 10.1111/j.1471-4159.1989.tb09140.x.
6
Postnatal changes in response to adenosine and adenine nucleotides in rat duodenum.大鼠十二指肠对腺苷和腺嘌呤核苷酸反应的产后变化。
Br J Pharmacol. 1989 Aug;97(4):1111-8. doi: 10.1111/j.1476-5381.1989.tb12568.x.
7
Involvement of inositol 1,4,5-trisphosphate and calcium in the action of adenine nucleotides on aortic endothelial cells.肌醇1,4,5 -三磷酸和钙在腺嘌呤核苷酸对主动脉内皮细胞作用中的参与情况。
J Biol Chem. 1987 Dec 25;262(36):17461-6.
8
Alpha-1 adrenoceptor-mediated positive inotropic effect and inositol trisphosphate increase in mammalian heart.α-1肾上腺素能受体介导的哺乳动物心脏正性肌力作用及三磷酸肌醇增加。
J Pharmacol Exp Ther. 1988 Apr;245(1):327-35.
9
Characterization of P2-purinoceptor mediated cyclic AMP formation in mouse C2C12 myotubes.小鼠C2C12肌管中P2嘌呤受体介导的环磷酸腺苷形成的特征分析
Br J Pharmacol. 1993 Sep;110(1):133-8. doi: 10.1111/j.1476-5381.1993.tb13782.x.
10
P2-, but not P1-purinoceptors mediate formation of 1, 4, 5-inositol trisphosphate and its metabolites via a pertussis toxin-insensitive pathway in the rat renal cortex.P2 - 嘌呤受体而非P1 - 嘌呤受体通过大鼠肾皮质中对百日咳毒素不敏感的途径介导1,4,5 - 三磷酸肌醇及其代谢产物的形成。
Br J Pharmacol. 1990 May;100(1):63-8. doi: 10.1111/j.1476-5381.1990.tb12052.x.

引用本文的文献

1
Positive Inotropic Effects of ATP Released the Maxi-Anion Channel in Langendorff-Perfused Mouse Hearts Subjected to Ischemia-Reperfusion.在经历缺血再灌注的Langendorff灌注小鼠心脏中,通过大阴离子通道释放的三磷酸腺苷的正性肌力作用
Front Cell Dev Biol. 2021 Jan 21;9:597997. doi: 10.3389/fcell.2021.597997. eCollection 2021.
2
The Ionotropic P2X4 Receptor has Unique Properties in the Heart by Mediating the Negative Chronotropic Effect of ATP While Increasing the Ventricular Inotropy.离子型P2X4受体在心脏中具有独特特性,它介导ATP的负性变时作用,同时增强心室收缩力。
Front Pharmacol. 2019 Sep 24;10:1103. doi: 10.3389/fphar.2019.01103. eCollection 2019.
3
Cardiac purinergic signalling in health and disease.健康与疾病中的心脏嘌呤能信号传导
Purinergic Signal. 2015 Mar;11(1):1-46. doi: 10.1007/s11302-014-9436-1. Epub 2014 Dec 20.
4
Could early ischemic arrhythmia triggered by purinergic activation of the transient receptor potential channels be prevented by creatine?肌酸能否预防由瞬时受体电位通道的嘌呤能激活引发的早期缺血性心律失常?
Exp Clin Cardiol. 2010 Winter;15(4):e104-8.
5
Contractile effects of adenosine, coronary flow and perfusion pressure in murine myocardium.腺苷对小鼠心肌的收缩作用、冠脉血流量及灌注压
Pflugers Arch. 2007 Jan;453(4):433-41. doi: 10.1007/s00424-006-0119-9. Epub 2006 Oct 28.
6
Imidapril treatment improves the attenuated inotropic and intracellular calcium responses to ATP in heart failure due to myocardial infarction.咪达普利治疗可改善心肌梗死所致心力衰竭中对ATP减弱的心肌收缩力和细胞内钙反应。
Br J Pharmacol. 2005 Jan;144(2):202-11. doi: 10.1038/sj.bjp.0705867.
7
Regulation of MAPK pathways in response to purinergic stimulation of adult rat cardiac myocytes.成年大鼠心肌细胞嘌呤能刺激反应中 MAPK 信号通路的调控
Mol Cell Biochem. 2003 Jan;242(1-2):163-71.
8
Purinoceptor-coupled Cl- channels in mouse heart: a novel, alternative pathway for CFTR regulation.小鼠心脏中嘌呤受体偶联的氯离子通道:一种新的、CFTR调节的替代途径。
J Physiol. 1999 Nov 15;521 Pt 1(Pt 1):43-56. doi: 10.1111/j.1469-7793.1999.00043.x.
9
P2 receptor subtypes in the cardiovascular system.心血管系统中的P2受体亚型。
Biochem J. 1998 Dec 15;336 ( Pt 3)(Pt 3):513-23. doi: 10.1042/bj3360513.
10
Purinergic stimulation of rat cardiomyocytes induces tyrosine phosphorylation and membrane association of phospholipase C gamma: a major mechanism for InsP3 generation.嘌呤能刺激大鼠心肌细胞可诱导酪氨酸磷酸化及磷脂酶Cγ的膜结合:这是肌醇三磷酸(InsP3)生成的主要机制。
Biochem J. 1996 Sep 1;318 ( Pt 2)(Pt 2):723-8. doi: 10.1042/bj3180723.

本文引用的文献

1
The physiological activity of adenine compounds with especial reference to their action upon the mammalian heart.腺嘌呤化合物的生理活性,特别涉及其对哺乳动物心脏的作用。
J Physiol. 1929 Nov 25;68(3):213-37. doi: 10.1113/jphysiol.1929.sp002608.
2
Effects of adenine nucleotides on the contractility and membrane potentials of rat atrium.腺嘌呤核苷酸对大鼠心房收缩性和膜电位的影响。
Circ Res. 1957 Jul;5(4):349-53. doi: 10.1161/01.res.5.4.349.
3
Lithium amplifies agonist-dependent phosphatidylinositol responses in brain and salivary glands.锂可增强大脑和唾液腺中激动剂依赖性磷脂酰肌醇反应。
Biochem J. 1982 Sep 15;206(3):587-95. doi: 10.1042/bj2060587.
4
8-phenyltheophylline: a potent P1-purinoceptor antagonist.8-苯基茶碱:一种强效的P1嘌呤受体拮抗剂。
Eur J Pharmacol. 1981 Oct 15;75(1):61-4. doi: 10.1016/0014-2999(81)90346-0.
5
Actions of adenosine and isoproterenol on isolated mammalian ventricular myocytes.腺苷和异丙肾上腺素对离体哺乳动物心室肌细胞的作用。
Circ Res. 1983 Sep;53(3):287-97. doi: 10.1161/01.res.53.3.287.
6
The effect of adenyl compounds on the rat heart.腺苷化合物对大鼠心脏的影响。
Br J Pharmacol. 1983 May;79(1):211-8. doi: 10.1111/j.1476-5381.1983.tb10514.x.
7
Isolated atrial myocytes: adenosine and acetylcholine increase potassium conductance.分离的心房肌细胞:腺苷和乙酰胆碱可增加钾离子电导。
Am J Physiol. 1983 May;244(5):H734-7. doi: 10.1152/ajpheart.1983.244.5.H734.
8
High levels of neuropeptide Y in peripheral noradrenergic neurons in various mammals including man.在包括人类在内的各种哺乳动物的外周去甲肾上腺素能神经元中,神经肽Y水平较高。
Neurosci Lett. 1983 Dec 2;42(2):167-72. doi: 10.1016/0304-3940(83)90401-9.
9
Interaction between adenosine and inotropic interventions in guinea pig atria.
Am J Physiol. 1983 Sep;245(3):H475-80. doi: 10.1152/ajpheart.1983.245.3.H475.
10
Source and concentration of extracellular adenosine triphosphate during haemostasis in rats, rabbits and man.大鼠、兔和人止血过程中细胞外三磷酸腺苷的来源和浓度
J Physiol. 1984 Sep;354:419-29. doi: 10.1113/jphysiol.1984.sp015385.

三磷酸腺苷(ATP)和其他腺嘌呤化合物可增强大鼠心脏的机械活动并增加三磷酸肌醇的生成。

ATP and other adenine compounds increase mechanical activity and inositol trisphosphate production in rat heart.

作者信息

Legssyer A, Poggioli J, Renard D, Vassort G

机构信息

Unité de Recherches de Physiologie Cellulaire Cardiaque INSERM U-241, Université Paris, Orsay, France.

出版信息

J Physiol. 1988 Jul;401:185-99. doi: 10.1113/jphysiol.1988.sp017157.

DOI:10.1113/jphysiol.1988.sp017157
PMID:3262739
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1191844/
Abstract
  1. The effects of adenosine 5'-triphosphate (ATP) and other adenine compounds were examined on rat papillary and right ventricular muscles in the presence of 10 microM-propranolol, 10 microM-atropine and 0.1 microM-prazosin or 10 microM-phentolamine. 2. Adenosine, adenosine 5'-monophosphate (AMP), adenosine 5'-diphosphate (ADP), ATP and alpha,beta-methylene ATP (APCPP) produced small positive inotropic effects, sometimes preceded by transient negative effects. 3. 8-Phenyltheophylline (8-PT), a P1-purinoceptor antagonist antagonized the negative effects and increased the positive inotropy induced by ATP and adenosine. 4. In the presence of APCPP, a P2-purinergic agonist, ATP had only negative inotropic effects. 5. Adenosine and ATP increased inositol 1, 4, 5- and inositol 1, 3, 4-trisphosphate as well as inositol mono- and bisphosphate formation. Maximal effects were obtained at concentrations of 0.5 mM. 6. APCPP increased inositol phosphate formation while 8-PT did not prevent the effects of adenosine and ATP. 7. It is suggested that P2-purinoceptor activation induces both a positive inotropy and an increase in inositol-lipid metabolism in rat ventricular muscles.
摘要
  1. 在存在10微摩尔普萘洛尔、10微摩尔阿托品和0.1微摩尔哌唑嗪或10微摩尔酚妥拉明的情况下,研究了5'-三磷酸腺苷(ATP)和其他腺嘌呤化合物对大鼠乳头肌和右心室肌的作用。2. 腺苷、5'-单磷酸腺苷(AMP)、5'-二磷酸腺苷(ADP)、ATP和α,β-亚甲基ATP(APCPP)产生小的正性肌力作用,有时之前会有短暂的负性作用。3. P1嘌呤受体拮抗剂8-苯基茶碱(8-PT)拮抗负性作用,并增强ATP和腺苷诱导的正性肌力作用。4. 在P2嘌呤能激动剂APCPP存在的情况下,ATP仅产生负性肌力作用。5. 腺苷和ATP增加了肌醇1,4,5-三磷酸和肌醇1,3,4-三磷酸以及肌醇单磷酸和双磷酸的形成。在0.5毫摩尔浓度时获得最大效应。6. APCPP增加了肌醇磷酸的形成,而8-PT并未阻止腺苷和ATP的作用。7. 提示P2嘌呤受体激活在大鼠心室肌中既诱导正性肌力作用,又诱导肌醇脂质代谢增加。