Advanced search
Start date
Betweenand
Related content
(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Participation of hepatic alpha/beta-adrenoceptors and AT(1) receptors in glucose release and portal hypertensive response induced by adrenaline or angiotensin II

Full text
Author(s):
de Araujo, L. J. T. [1] ; Nagaoka, M. R. [2] ; Borges, D. R. [3] ; Kouyoumdjian, M. [1]
Total Authors: 4
Affiliation:
[1] Univ Fed Sao Paulo, Dept Bioquim, Escola Paulista Med, Sao Paulo, SP - Brazil
[2] Univ Fed Sao Paulo, Dept Biociencias, Baixada Santista, SP - Brazil
[3] Univ Fed Sao Paulo, Dept Med, Escola Paulista Med, Sao Paulo, SP - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Brazilian Journal of Medical and Biological Research; v. 51, n. 12 2018.
Web of Science Citations: 2
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 (AT(1)) and adrenergic (proportional to 1- and beta-) receptors (AR) belong to the G-proteins superfamily, which signaling promote glycogen breakdown and glucose release. Interactive relationship between AR and AT(1)-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 All and adrenaline (Adr) in the presence of AT(1) (losartan) and proportional to 1-AR and beta-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 proportional to(1)-AR. A significant decrease in the hemodynamic response induced by Adr caused by losartan confirmed the participation of AT(1)-R. The metabolic response induced by AII was impaired by propranolol, indicating the participation of beta-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 All effects. This possible cross-talk between beta-AR and AT(1)-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