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Reports |
From the Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, Argentina.
Correspondence to Dr Ernesto A. Aiello or Dr Horacio E. Cingolani, Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, 60 y 120, La Plata 1900, Argentina. E-mail cicme{at}atlas.med.unlp.edu.ar
Abstract
The goal of the present study was to evaluate the effects of Ang II on the current produced by the Na+-Ca2+ exchanger (INCX) working in the reverse mode and the possible autocrine role played by the release of endothelin (ET) in these actions. INCX was studied in isolation in cat cardiac myocytes. Angiotensin II (Ang II) (100 nmol/L) increased INCX 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 INCX 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 INCX is the result of the autocrine actions of ET released by the octapeptide.
Key Words: sodium-calcium exchanger cardiac myocytes angiotensin II endothelin
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