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Cui TX, Iwai M, Hamai M, et al. Receptor subtype mediating the action of circulating endothelin on glucose metabolism and hemodynamics in perfused rat liver. Regul Pept. 1999;83(2):117-22doi: 10.1016/s0167-0115(99)00058-0.
Cui, T. X., Iwai, M., Hamai, M., & Shimazu, T. (1999). Receptor subtype mediating the action of circulating endothelin on glucose metabolism and hemodynamics in perfused rat liver. Regulatory peptides, 83(2), 117-22. https://doi.org/10.1016/s0167-0115(99)00058-0
Cui, T X, et al. "Receptor subtype mediating the action of circulating endothelin on glucose metabolism and hemodynamics in perfused rat liver." Regulatory peptides vol. 83,2 (1999): 117-22. doi: https://doi.org/10.1016/s0167-0115(99)00058-0
Cui TX, Iwai M, Hamai M, Shimazu T. Receptor subtype mediating the action of circulating endothelin on glucose metabolism and hemodynamics in perfused rat liver. Regul Pept. 1999 Sep 15;83(2):117-22. doi: 10.1016/s0167-0115(99)00058-0. PMID: 10511465.
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Regul Pept. 1999 Sep 15;83(2):117-22. doi: 10.1016/s0167-0115(99)00058-0.

Receptor subtype mediating the action of circulating endothelin on glucose metabolism and hemodynamics in perfused rat liver.

Regulatory peptides

T X Cui, M Iwai, M Hamai, T Shimazu

Affiliations

  1. Department of Medical Biochemistry, Ehime University School of Medicine, Shigenobu, Japan.

PMID: 10511465 DOI: 10.1016/s0167-0115(99)00058-0

Abstract

The subtype of endothelin receptor that mediates metabolic and hemodynamic effects of circulating endothelin was explored using perfused rat liver. Infusion of endothelin (ET)-1 or ET-3 into the portal vein at a concentration of 0.3 nM increased glucose and lactate output and decreased perfusion flow, although ET-3 was less effective than ET-1. The metabolic effects of ET-1 were observed even under costant-flow perfusion. Infusion of either sarafotoxin S6b or S6c, an ET(A)- or ET(B)-receptor agonist, mimicked the actions of ET-1 to an equal extent. The flow reduction and glucose production induced by ET-1 were partly attenuated by the ET(A)-receptor antagonist BQ485. By contrast, ET(B)-receptor antagonist BQ788 enhanced glucose production caused by ET-1 and ET-3 without affecting the hemodynamic change. The effects of ET-1 and ET-3 were almost totally inhibited by the combination of BQ485 and BQ788. These results suggest that both ET(A) and ET(B) receptors are involved in the metabolic and hemodynamic effects of circulating endothelin in rat liver, while the ET(A)-receptor-mediated action appears to be dominant.

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