The Role of Calcium-Sensing Receptors in Endothelin-1-Dependent Effects on Adult Rat Ventricular Cardiomyocytes: Possible Contribution to Adaptive Myocardial Hypertrophy

2017 ◽  
Vol 232 (9) ◽  
pp. 2508-2518 ◽  
Author(s):  
Elena Dyukova ◽  
Rolf Schreckenberg ◽  
Christoph Arens ◽  
Guzel Sitdikova ◽  
Klaus-Dieter Schlüter
1997 ◽  
Vol 273 (5) ◽  
pp. E922-E931 ◽  
Author(s):  
M. C. Rebsamen ◽  
D. J. Church ◽  
D. Morabito ◽  
M. B. Vallotton ◽  
U. Lang

The mechanism of endothelin-1 (ET-1)-induced atrial natriuretic peptide (ANP) release was studied in neonatal rat ventricular cardiomyocytes. These cells expressed a single high-affinity class of ETAreceptor (dissociation constant = 54 ± 18 pM, n = 3), but no ETB receptors. Incubation of cardiomyocytes with ET-1 led to concentration-dependent ANP release and prostacyclin production. ET-1-induced ANP release was affected by neither protein kinase C (PKC) inhibition or downregulation nor by cyclooxygenase inhibition, indicating that ET-1-stimulated ANP secretion is not a PKC-mediated, prostaglandin-dependent process. Furthermore, ET-1 significantly stimulated adenosine 3′,5′-cyclic monophosphate (cAMP) production and increased cytosolic calcium concentration in these preparations. Both ET-1-induced calcium influx and ANP release were decreased by the cAMP antagonist Rp-cAMPS, the Rp diastereoisomer of cAMP. Moreover, ET-1-induced ANP secretion was strongly inhibited in the presence of nifedipine as well as in the absence of extracellular calcium. Thus our results suggest that ET-1 stimulates ANP release in ventricular cardiomyocytes via an ETAreceptor-mediated pathway involving cAMP formation and activation of a nifedipine-sensitive calcium channel.


2011 ◽  
Vol 59 (S 01) ◽  
Author(s):  
B Ziegelhöffer ◽  
A Busch ◽  
A Dietze ◽  
A Rastan ◽  
M Kostelka ◽  
...  
Keyword(s):  

2015 ◽  
Vol 1 ◽  
pp. 199-209 ◽  
Author(s):  
Nabila Yousef Abdel Haleem ◽  
Hoda Mahmoud El-Aasar ◽  
Sherif Mohamed Zaki ◽  
Sherif Mohamed Sabry ◽  
Ahmed Wafiq El-Zainy

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