Pharmacological hypothesis: Nitric oxide‐induced inhibition of ADAM‐17 activity as well as vesicle release can in turn prevent the production of soluble endothelin‐converting enzyme
Abstract:Endothelin‐1 (ET‐1) and nitric oxide (NO) are two highly potent vasoactive molecules with opposing effects on the vasculature. Endothelin‐converting enzyme (ECE) and nitric oxide synthase (NOS) catalyse the production of ET‐1 and NO, respectively. It is well established that these molecules play a crucial role in the initiation and progression of cardiovascular diseases and have therefore become targets of therapy. Many studies have examined the mechanism(s) by which NO regulates ET‐1 production. Expression an… Show more
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