Preliminary reportNeutral endopeptidase inhibition increases the urinary excretion and plasma levels of endothelin☆
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Cited by (49)
Natriuretic peptides and cardio-renal disease
2014, International Journal of CardiologyCitation Excerpt :ANP and CNP are the NPs most susceptible to degradation by NEP, whereas the enzyme has a lower affinity for BNP [46]. NEP also degrades other vasoactive peptides including vasodilators, e.g. substance P and bradykinin, and vasoconstrictors such as ET-1 and Ang II [47–51]. Consequently, the net physiological effect of NEP will depend on the balance between its actions on vasodilators versus vasoconstrictors.
Effects of Endopeptidase Inhibition on the Contraction-Relaxation Response of Isolated Human Vaginal Tissue
2013, Journal of Sexual MedicineCitation Excerpt :The enzyme shares a structural similarity with the so‐called endothelin‐converting enzyme (ECE) and was initially isolated from renal epithelial brush border cells. However, it is also expressed in vascular endothelial and smooth muscle cells [6-10]. In addition to the degradation of vasoactive peptides, NEP also catalyzes the conversion of big endothelin‐1 (Big ET‐1) into ET‐1, a potent vasoconstrictor peptide [11].
Neutral endopeptidase (EC 3.4.24.11) in cirrhotic liver: A new target to treat portal hypertension?
2005, Journal of HepatologyUpregulation of vascular renin-angiotensin and endothelin systems in rats inhibited of nitric oxide synthesis
2002, Pharmacological ResearchInhibition of neointima formation in an organ culture of human saphenous vein: A comparison of dual endothelin-converting enzyme/neutral endopeptidase and selective neutral endopeptidase inhibition
2001, Journal of Vascular SurgeryCitation Excerpt :In conditions characterized by neointima formation, such as arterial bypass grafting, treatment with a dual ECE/NEP inhibitor is likely to compound the clinical problem. Because ET-1 is a substrate for NEP,12 inhibition of NEP will actually raise ET-1 levels. Any studies with dual inhibitors will, by their very nature, be complicated because the observed response could be caused by ECE inhibition, NEP inhibition, or both.
Pharmacology and cardiovascular implications of the kinin-kallikrein system
1999, Japanese Journal of Pharmacology
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