CIC   05421
CENTRO DE INVESTIGACIONES CARDIOVASCULARES "DR. HORACIO EUGENIO CINGOLANI"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Hypotonic Swelling Promotes Nitric Oxide Release in Rat Cardiac Ventricular Myoycte: Impact on Swelling-Induced Negative Inotropic Effect.
Autor/es:
LUIS GONANO; MALENA MORELL; MARTIN VILA PETROFF
Lugar:
New London
Reunión:
Congreso; Gordon Research Conferences, Cardiac Regulatory Mechanism, New London, USA. Junio 2012.; 2012
Resumen:
Hypotonic Swelling Promotes Nitric Oxide Release in Rat Cardiac Ventricular Myoycte: Impact on Swelling-Induced Negative Inotropic Effect. Luis Gonano, Malena Morell, Marisa SepĂșlveda and Martin Vila Petroff. Centro de Investigaciones Cardiovasculares CCT-CONICET. Facultad de Cs. MĂ©dicas, UNLP. 60 y 120 La Plata, Argentina.   Cell swelling is known to contribute to the pathophysiology of ischemia and reperfusion by promoting contractile dysfunction and predisposing the heart for arrhythmias.  However, the underlying subcellular mechanisms of swelling-induced contractile dysfunction are still not fully understood. We have previously shown that cardiac cell stretch promotes nitric oxide (NO) release favoring spontaneous SR Ca2+ release. Here we investigate whether hypotonic swelling promotes nitric oxide release and if so, whether it contributes to cardiac cell swelling-induced contractile dysfunction.  Treating rat cardiac myocytes, loaded with the NO sensor DAF-2, with a hypotonic solution, increased cell volume, reduced myocyte contraction amplitude and significantly increased DAF-2 fluorescence. When cells were exposed to the hypotonic solution supplemented with 2.5 mM of the NO synthase inhibitor L-Name, cell swelling occurred in the absence of NO release. Interestingly, swelling-induced negative inotropic effect was exacerbated in the presence of L-Name. These results suggest that hypotonic swelling promotes NO release which reduces contractile dysfunction. Taken together, these findings suggest a novel mechanism for NO release in cardiac myocytes with putative pathophysiological relevance in the context of ischemia and reperfusion, where it may serve a cardioprotective role by reducing the extent of contractile dysfunction.
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