Autocrine stimulation of cardiac Na+-Ca2+ exchanger currents by endogenous endothelin released by angiotensin II
The goal of the present study was to evaluate the effects of Ang II on the current produced by the Na<SUP>+</SUP>-Ca<SUP>2+</SUP> exchanger (I<SUB>NCX</SUB>) working in the reverse mode and the possible autocrine role played by the release of endothelin (ET) in th...
Guardado en:
| Autores principales: | , , |
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| Formato: | Articulo Comunicacion |
| Lenguaje: | Inglés |
| Publicado: |
2002
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| Materias: | |
| Acceso en línea: | http://sedici.unlp.edu.ar/handle/10915/84668 |
| Aporte de: |
| Sumario: | The goal of the present study was to evaluate the effects of Ang II on the current produced by the Na<SUP>+</SUP>-Ca<SUP>2+</SUP> exchanger (I<SUB>NCX</SUB>) working in the reverse mode and the possible autocrine role played by the release of endothelin (ET) in these actions. I<SUB>NCX</SUB> was studied in isolation in cat cardiac myocytes. Angiotensin II (Ang II) (100 nmol/L) increased I<SUB>NCX</SUB> at potentials higher than 0 mV (at +60 mV: 2.07±0.22 pA/pF in control versus 2.73±0.22 pA/pF in Ang II, n = 9; P < 0.05). The increase in I<SUB>NCX</SUB> induced by Ang II was prevented by the treatment of the cells with the unspecific blocker of the ET receptors, TAK 044 (1 μmol/L) (at +60 mV: 2.15±0.27 pA/pF in control versus 2.01±0.26 pA/pF in Ang II, n=5, NS). These results show, for the first time, that the effect of Ang II on I<SUB>NCX</SUB> is the result of the autocrine actions of ET released by the octapeptide. |
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