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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
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 c...
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| Publicat a: | Pharmacol Res Perspect |
|---|---|
| Autors principals: | , , , |
| Format: | Artigo |
| Idioma: | Inglês |
| Publicat: |
John Wiley and Sons Inc.
2017
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| Matèries: | |
| Accés en línia: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5625149/ https://ncbi.nlm.nih.gov/pubmed/28971608 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1002/prp2.335 |
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