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Nitric oxide mediates protective effect of endothelin receptor antagonism during myocardial ischemia and reperfusion
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- Gonon, AT (author)
- Karolinska Institutet
- Erbas, D (author)
- Broijersen, A (author)
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- Valen, G (author)
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- (creator_code:org_t)
- American Physiological Society, 2004
- 2004
- English.
- In: American journal of physiology. Heart and circulatory physiology. - : American Physiological Society. - 0363-6135 .- 1522-1539. ; 286:5, s. H1767-H1774
- Journal article (peer-reviewed)
Abstract
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- Endothelin (ET) receptor antagonism protects from ischemiareperfusion injury. We hypothesized that the cardioprotective effect is related to nitric oxide (NO) bioavailability. Buffer-perfused rat and mouse hearts were subjected to ischemia and reperfusion. At the onset of ischemia, the rat hearts received vehicle, the dual endothelin type A/type B (ETA/ETB) receptor antagonist bosentan (10 μM), the NO synthase inhibitor NG-monomethyl-l-arginine (l-NMMA; 100 μM), the combination of bosentan and l-NMMA or the combination of bosentan, l-NMMA, and the NO substrate l-arginine (1 mM). Hearts from wild-type and endothelial NO synthase (eNOS)-deficient mice received either vehicle or bosentan. Myocardial performance, endothelial function, NO outflow, and eNOS expression were monitored. Bosentan significantly improved myocardial function during reperfusion in rats and in wild-type mice, but not in eNOS-deficient mice. The functional protection afforded by bosentan was inhibited by l-NMMA, whereas it was restored by l-arginine. Myocardial expression of eNOS (immunoblotting) increased significantly in bosentan-treated rat hearts compared with vehicle hearts. Recovery of NO outflow during reperfusion was enhanced in the bosentan-treated rat heart. The endothelium-dependent vasodilator adenosine diphosphate increased coronary flow by 18 ± 9% at the end of reperfusion in the bosentan group, whereas it reduced coronary flow by 7 ± 5% in the vehicle group ( P < 0.001). The response to the endothelium-independent dilator sodium nitroprusside was not different between the two groups. In conclusion, the dual ETA/ETB receptor antagonist bosentan preserved endothelial and cardiac contractile function during ischemia and reperfusion via a mechanism dependent on endothelial NO production.
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