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Omapatrilat: still a promise in salt-sensitive hypertension?

Omapatrilat inhibits both angiotensin-converting enzyme (ACE) and neutral endopeptidase [1]. Because neutral endopeptidase metabolizes vasodilator peptides, including natriuretic peptide, adrenomedullin and bradykinin, omapatrilat has been proposed as a more effective agent in reversing both hypertension and its associated cardiovascular complications compared to ACE inhibitors. Moreover, because angiotensin II plays little effect in maintaining hypertension in common volume-dependent forms, it may have a much extended efficacy within the hypertensive population. In a contemporary study of patients with salt-sensitive hypertension, Ferrario et al. [2] showed that omapatrilat was almost twice as effective as lisinopril in reducing blood pressure. In this issue of the journal, Millette et al. [3] tested these concepts by contrasting omapatrilat and lisinopril on blood pressure, morphological vascular changes, endothelial function and overall survival in a deoxycorticosterone (DOCA)-salt hypertensive rat model. Surprisingly, there was a similar modest reduction in blood pressure with both agents. Similarly, both agents reduced media thickness in the small coronary arterioles and reduced aortic superoxide formation to the same extent. However, despite these similar effects on blood pressure and blood vessels, omapatrilat drastically reduced mortality in the severe model of DOCA-salt hypertension (12.5%), whereas the mortality with lisinopril (75.0%) was similar to that in non-treated control rats (87.5%).