Endothelin-1 inhibits L-type Ca2+ current enhanced by isoprenaline in rat atrial myocytes.
Endothelin-1 inhibits L-type Ca2+ current enhanced by isoprenaline in rat atrial myocytes.
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Endothelin-1 抑制大鼠心房肌细胞中异丙肾上腺素增强的 L 型 Ca2 电流。
DOI：
10.1097/00005344-199701000-00021
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发表时间：
1997
影响因子：
3
通讯作者：
D. Potreau
中科院分区：
文献类型：
--
作者：
N. Delpech;H. Soustre;D. Potreau
内皮素-1 （ET-1）通过复杂的信号通路发挥直接的心脏作用，并与调节心脏活动的神经递质相互作用。采用膜片钳技术研究ET-1对心脏l型Ca2+电流（ICaL）对离体大鼠心房肌细胞β -肾上腺素能刺激的影响。ET-1 （5 × 10(-8) M）逆转了异丙肾上腺素（10(-6)M）诱导的ICaL升高，但对基础ICaL和（-）Bay k8644 （10(-6) M）升高的ICaL没有影响；所以ET-1可能只有在Ca2+通道被磷酸化时才会发挥作用。被BQ-123 （10(-6) M）阻断且不受IRL 1038 （3.5 x 10(-8) M）影响的ET-1的抗肾上腺素能作用应由ET-A受体介导。当在异丁基甲基黄嘌呤（IBMX; 10(-6) M）存在的情况下，用forskolin （3 × 10(-6) M）、8-溴环腺苷单磷酸（8-Br-cAMP； 200微米）或cAMP（100微米）增加ICaL时，仍能观察到ET-1的抑制作用，这表明ET-1对ICaL的抗肾上腺素能作用独立于cAMP依赖的磷酸化途径。已知ET-1是磷酸肌苷水解的激活剂，导致IP3和二酰基甘油（DAG）的产生增加。在ET-1的作用中，可能不存在Ca（2+）依赖性的ICaL抑制，从而通过IP3导致细胞内Ca2+池的升高，因为在试管内培养基中存在EGTA。在蛋白激酶C抑制剂[PKC]存在的情况下，ET-1逆转异丙肾上腺素诱导的ICaL增加（19-31）；100微米)，使得dag依赖性的PKC激活不太可能参与。因此ET-1的抗肾上腺素能作用也可能不依赖于磷酸肌苷途径。
Endothelin-1 (ET-1) was shown to exert direct cardiac effects by complex signaling pathways and to interact with neurotransmitter regulation of cardiac activity. The effect of ET-1 was investigated on the beta-adrenergic stimulation of cardiac L-type Ca2+ current (ICaL) on isolated rat atrial myocytes by using the patch-clamp technique. ET-1 (5 x 10(-8) M) reversed the increase in ICaL induced by isoprenaline (10(-6) M) but had no effect on basal ICaL and on (-) Bay K 8644-increased ICaL (10(-6) M); so ET-1 might exert an effect only when the Ca2+ channels are phosphorylated. The antiadrenergic action of ET-1, blocked by BQ-123 (10(-6) M) and unaffected by IRL 1038 (3.5 x 10(-8) M) should be mediated by ET-A receptors. The inhibitory action of ET-1 was still observed when ICaL was previously increased by forskolin (3 x 10(-6) M), 8-bromo-cyclic adenosine monophosphate (8-Br-cAMP; 200 microM), or cAMP (100 microM) in presence of isobutyl methyl xanthine (IBMX; 10(-6) M), suggesting that the antiadrenergic action of ET-1 on ICaL was exerted independent of the cAMP-dependent phosphorylation pathway. ET-1 is known to be an activator of phosphoinositide hydrolysis, resulting in an increased production of IP3 and diacylglycerol (DAG). A Ca(2+)-dependent inhibition of ICaL consequently to an elevation of the intracellular Ca2+ pool via IP3 might be excluded in the action of ET-1, because of the presence of EGTA in the intrapipette medium. ET-1 reversed the isoprenaline-induced increase in ICaL in the presence of protein kinase C inhibitor [PKC(19-31); 100 microM), making unlikely the involvement of a DAG-dependent activation of PKC. Therefore the antiadrenergic action of ET-1 might also be independent on the phosphoinositide pathway.
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DOI：
--
发表时间：
1994-06
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Michel Pucéat;R. Hilal-Dandan;B. Strulovici;L. Brunton;Joan Heller Brown
通讯作者：
Michel Pucéat;R. Hilal-Dandan;B. Strulovici;L. Brunton;Joan Heller Brown
DOI：
--
发表时间：
1990-11
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
H. Shubeita;Patrick M. McDonough;A. N. Harris;Kirk U. Knowlton;C. C. Glembotski-C.;Joan Heller Brown;Kenneth R. Chien
通讯作者：
H. Shubeita;Patrick M. McDonough;A. N. Harris;Kirk U. Knowlton;C. C. Glembotski-C.;Joan Heller Brown;Kenneth R. Chien
毛喉素和乙酰胆碱对单个离体心肌细胞钙电流的影响。
影响因子：
3.6
作者：
Hartzell,HC;Fischmeister,R
通讯作者：
Fischmeister,R
影响因子：
15.9
作者：
KELLY, RA;EID, H;SMITH, TW
通讯作者：
SMITH, TW
内皮素刺激原代心房肌细胞分泌心房钠尿因子需要蛋白激酶 C 和钙调蛋白激酶。
DOI：
--
发表时间：
1992
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Irons,CE;Sei,CA;Hidaka,H;Glembotski,CC
通讯作者：
Glembotski,CC