Key result
The rabbit aorta generates ET-1(1-31) from exogenous BigET-1 via a chymase-like enzyme when ECE and NEP are inhibited, with NEP being the predominant pathway for its cleavage to a bioactive metabolite.
Population
Endothelium-intact rabbit aortic rings and tissue from heart, lung, kidney, and liver
Comparison
Exogenous big endothelin-1 with or without… vs Control conditions without specific inhibitors
Design
Preclinical
Authors
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Preclinical rabbit aorta data on ET-1(1-31) pathways should not alter practice; leaves open chymase-NEP roles in human ET metabolism.
This preclinical study elucidates the enzymatic pathways, specifically involving chymase-like enzymes and NEP, responsible for generating and metabolizing ET-1(1-31) in rabbit vasculature.
Tirapelli et al. (2006) studied this question. BigET-1 and enzymatic inhibitors was evaluated on Vascular contraction and generation of ET-1(1-31). The rabbit aorta generates ET-1(1-31) from exogenous BigET-1 via a chymase-like enzyme when ECE and NEP are inhibited, with NEP being the predominant pathway for its cleavage to a bioactive metabolite.
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