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(Reference retrieved automatically from SciELO through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Participation of hepatic α/β-adrenoceptors and AT1 receptors in glucose release and portal hypertensive response induced by adrenaline or angiotensin II

Full text
Author(s):
L.J.T. de Araújo [1] ; M.R. Nagaoka [2] ; D.R. Borges [3] ; M. Kouyoumdjian [4]
Total Authors: 4
Affiliation:
[1] Universidade Federal de São Paulo. Departamento de Bioquímica, Escola Paulista de Medicina - Brasil
[2] Universidade Federal de São Paulo. Departamento de Biociências - Brasil
[3] Universidade Federal de São Paulo. Departamento de Medicina, Escola Paulista de Medicina - Brasil
[4] Universidade Federal de São Paulo. Departamento de Bioquímica, Escola Paulista de Medicina - Brasil
Total Affiliations: 4
Document type: Journal article
Source: Brazilian Journal of Medical and Biological Research; v. 51, n. 12 2018-11-14.
Abstract

It has been previously demonstrated that the hemodynamic effect induced by angiotensin II (AII) in the liver was completely abolished by losartan while glucose release was partially affected by losartan. Angiotensin II type 1 (AT1) and adrenergic (∝1- and β-) receptors (AR) belong to the G-proteins superfamily, which signaling promote glycogen breakdown and glucose release. Interactive relationship between AR and AT1-R was shown after blockade of these receptors with specific antagonists. The isolated perfused rat liver was used to study hemodynamic and metabolic responses induced by AII and adrenaline (Adr) in the presence of AT1 (losartan) and ∝1-AR and β-AR antagonists (prazosin and propranolol). All antagonists diminished the hemodynamic response induced by Adr. Losartan abolished hemodynamic response induced by AII, and AR antagonists had no effect when used alone. When combined, the antagonists caused a decrease in the hemodynamic response. The metabolic response induced by Adr was mainly mediated by ∝1-AR. A significant decrease in the hemodynamic response induced by Adr caused by losartan confirmed the participation of AT1-R. The metabolic response induced by AII was impaired by propranolol, indicating the participation of β-AR. When both ARs were blocked, the hemodynamic and metabolic responses were impaired in a cumulative effect. These results suggested that both ARs might be responsible for AII effects. This possible cross-talk between β-AR and AT1-R signaling in the hepatocytes has yet to be investigated and should be considered in the design of specific drugs. (AU)

FAPESP's process: 11/13974-8 - Vasoactive peptides action in the liver of rats submitted to different experimental models of disease
Grantee:Maria Kouyoumdjian
Support Opportunities: Regular Research Grants