Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Ros, M.N. et al.

Endothelin 1 versus endothelin 3 in the development of the slow force response to myocardial stretch.

BACKGROUND: Myocardial stretch promotes an increase in developed force (DF) in two phases: a rapid initial phase, and a slowly developing second phase called the slow force response (SFR) to myocardial stretch. The SFR results from an autocrine/paracrine mechanism of angiotensin II and endothelin (ET) release that is triggered by the stretch. OBJECTIVE: To explore whether exogenous ET-1 and/or ET-3 could mimic the SFR. METHODS: Experiments were performed in isometrically contracting (0.2 Hz) rat papillary muscles at 30 degrees C. DF was measured either after stretch or after the addition of ET-1 or ET-3 (in doses that increase contractility to a similar magnitude as does the SFR), with or without the selective ETA receptor antagonist BQ123 (300 nmol/L). RESULTS AND CONCLUSIONS: After 15 min, the SFR was 17.6+/-1.4% greater than the initial rapid phase (n=4; P<0.05) and was abolished by BQ123. ET-1 (5.0 nmol/L) increased DF by 25.9+/-1.7% (n=4; P<0.05) after 30 min, an effect that was not altered by BQ123 (22.6+/-3.9%; n=5). ET-3 (5.0 nmol/L) increased DF by 23.8+/-3.2% (n=5; P<0.05), an effect that was suppressed by BQ123 (-5.4+/-1.9%; n=5; P<0.05). Given that BQ123 eliminated the SFR and the inotropic response to ET-3 but not to ET-1, the results suggest that the SFR that follows myocardial stretch is due to the endogenous release of ET-3 acting in an autocrine/paracrine fashion.[1]

References

Endothelin 1 versus endothelin 3 in the development of the slow force response to myocardial stretch. Ros, M.N., Dulce, R.A., Pérez, N.G., Camilión de Hurtado, M.C., Cingolani, H.E. The Canadian journal of cardiology. (2005) [Pubmed]

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