Telmisartan, an angiotensin II type 1 receptor antagonist, attenuates T-type Ca2+ channel expression in neonatal rat cardiomyocytes

2009 ◽  
Vol 609 (1-3) ◽  
pp. 105-112 ◽  
Author(s):  
Masaki Morishima ◽  
Yan Wang ◽  
Yuko Akiyoshi ◽  
Shinji Miyamoto ◽  
Katsushige Ono
2003 ◽  
Vol 284 (4) ◽  
pp. H1269-H1276 ◽  
Author(s):  
Pinggang Liu ◽  
Derek A. Misurski ◽  
Venkat Gopalakrishnan

With the use of fura 2 measurements in multiple and single cells, we examined whether cysteinyl leukotrienes (CysLT) mediate angiotensin II (ANG II)-evoked increases in cytosolic free Ca2+ concentration ([Ca2+]i) in neonatal rat cardiomyocytes. ANG II-evoked CysLT release peaked at 1 min. The angiotensin type 1 (AT1) antagonist losartan, but not the AT2antagonist PD-123319, attenuated the elevations in [Ca2+]i and CysLT levels evoked by ANG II. Vasopressin and endothelin-1 increased [Ca2+]i but not CysLT levels. The 5-lipoxygenase (5-LO) inhibitor AA-861 and the CysLT1-selective antagonist MK-571 reduced the maximal [Ca2+]i responses to ANG II but not to vasopressin and endothelin-1. While MK-571 reduced the responses to leukotriene D4 (LTD4), the dual CysLT antagonist BAY-u9773 completely blocked the [Ca2+]i elevation to both LTD4and LTC4. These data confirm that ANG II-evoked increases, but not vasopressin- and endothelin-1-evoked increases, in [Ca2+]i involve generation of the 5-lipoxygenase metabolite CysLT. The inositol (1,4,5)-trisphosphate [Ins(1,4,5)P3] antagonist 2-aminoethoxydiphenyl borate attenuated the [Ca2+]i responses to ANG II and LTD4. Thus AT1 receptor activation by ANG II is linked to CysLT-mediated Ca2+ release from Ins(1,4,5)P3-sensitive intracellular stores to augment direct ANG II-evoked Ca2+ mobilization in rat cardiomyocytes.


2005 ◽  
Vol 67 (2) ◽  
pp. 216-224 ◽  
Author(s):  
N LALEVEE ◽  
M REBSAMEN ◽  
S BARRERELEMAIRE ◽  
E PERRIER ◽  
J NARGEOT ◽  
...  

2013 ◽  
Vol 37 (8) ◽  
pp. 689-694 ◽  
Author(s):  
Gianluca Lucchese ◽  
Giulia Elisa Cambi ◽  
Fabrizio De Rita ◽  
Mauro Franzoi ◽  
Giuseppe Faggian ◽  
...  

2003 ◽  
Vol 81 (2) ◽  
pp. 79-83 ◽  
Author(s):  
Gerd Wallukat ◽  
Dajana Neichel ◽  
Eberhard Nissen ◽  
Volker Homuth ◽  
Friedrich C Luft

We showed that sera from patients with preeclampsia contain autoantibodies directed against the angiotensin II AT1 receptor. The antibodies recognize an epitope on the second extracellular loop of the receptor and are immuno globulins of the IgG3 subclass. The antibodies accelerate the beating rate of neonatal rat cardiomyocytes. The agonistic effect can be blocked with the AT1 receptor blocker losartan and can be neutralized by a peptide corresponding to the AT1 receptor's second extracellular loop. In further studies we shown that the autoantibodies recognize a specific conformation of the AT1 receptor. Cleavage of the external disulfide bond with dithiothreitol caused an inactivation of the receptor when stimulated either with Ang II or the autoantibodies in a system of cultured neonatal rat cardiomyocytes. Long-term stimulation of the AT1 receptor with either agonists down-regulated the AT1 receptor-mediated response to a second Ang II stimulation. These observations show that the agonistic autoantibodies behave pharmacologically in a similar fashion to Ang II. We have found the autoantibodies in all women meeting the clinical criteria of preeclampsia and suggest that they may be important to the pathogenesis of the disease.Key words: angiotensin II, preeclampsia, autoantibodies, IgG subclasses, dithiotrietol, AT1 receptor.


1997 ◽  
Vol 121 (1) ◽  
pp. 118-124 ◽  
Author(s):  
Klaus Pönicke ◽  
Ingrid Heinroth-Hoffmann ◽  
Karin Becker ◽  
Otto-Erich Brodde

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