Why the study?
Do endothelin receptor antagonists reduce blood pressure and prevent end-organ damage in hypertension?
Do endothelin receptor antagonists reduce blood pressure and prevent end-organ damage in hypertension?
Endothelin receptor antagonists show promise in preclinical models for reducing blood pressure and preventing end-organ damage in hypertension, warranting further clinical investigation.
Supports clinical trials of ET-receptor antagonists in hypertension; leaves open reversal of established end-organ damage.
Excitement always greets the development of a new class of therapeutic drug, representing as it does the combined efforts of the pharmaceutical industry, research laboratories and clinicians. Endothelin (ET)-receptor antagonists are being actively developed as new therapeutic agents for cardiovascular diseases, and may also be of use in other pathological conditions. Based on early and indirect evidence, ET has been implicated in the pathophysiology of hypertension; the receptor antagonists have been studied quite extensively in this setting at the preclinical level. We now possess direct evidence that such drugs are effective as antihypertensives in some experimental models of hypertension. Furthermore, the ability of ET-receptor antagonists to prevent hypertension-induced end-organ damage is also well documented. Their capacity to reverse already established target organ alterations remains poorly defined. Based on our current preclinical and clinical knowledge, this review presents the anticipated clinical usefulness of these new drugs, both in terms of blood pressure reduction and the protection of target organs.
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A 1999 study studied this question.
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