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Endothelins and cardiac fibrosis.

To the Editor: 

In the March issue of Hypertension , Dr Hocher and colleagues reported on the role of the endothelin (ET) system in the cardiac remodeling of renovascular hypertension.1 According to their findings, both fibrosis of the left ventricle (LV) and hypertrophy of intracardiac arteries were markedly prevented in the 2-kidney, 1-clip (2K1C) rat model, although they found changes neither in the cardiac tissue content of immunoreactive (ir) ET-1 and bigET-1 nor in the cardiac expression of the endothelin ETA and ETB receptors, both in the early (10 days) and in the later (4 and 12 weeks) stages after clipping one renal artery. Interestingly, since these effects occurred in spite of the lack of any blood pressure (BP) lowering effect, the authors proposed that the ET system contributes to myocardial fibrosis and arterial hypertrophy via BP-independent mechanisms. Furthermore, on the basis of the differential results obtained with the ETA antagonist BQ-123 and with an ETB antagonist IRL-1038, both administered daily intraperitoneally, they concluded that the ETA receptor is involved in wall hypertrophy of intracardiac arteries while the ETB plays a role in fibrosis. Although these findings are interesting and obviously important for our understanding of the mechanisms of these common adverse effects of hypertension on the heart, they deserve some comments.

In a recent paper, which Dr Hocher and colleagues quoted twice (References 9 and 33), Dr Mulder and colleagues reported that the mixed ETA/ETB receptor antagonist bosentan, administered orally at the same dosage of Dr Hocher and colleagues, dramatically reduced mortality and myocardial fibrosis in a rat model of congestive heart failure.2 They suggested an involvement of the ETA receptor in such detrimental effect of ET-1, in keeping with the results of Nguyen and colleagues, with …