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.)

Insulin alone or with captopril: effects on signaling pathways (AKT and AMPK) and oxidative balance after ischemia-reperfusion in isolated hearts

Full text
Author(s):
de Oliveira, Ubirajara Oliveira [1, 2] ; Bello-Kein, Adriane [1] ; de Oliveira, Alvaro Reischak [3] ; Kuchaski, Luiz Carlos [2] ; Machado, Ubiratan Fabres [4] ; Irigoyen, Maria Claudia [1, 5] ; Schaan, Beatriz D'Agord [6]
Total Authors: 7
Affiliation:
[1] Univ Fed Rio Grande do Sul, ICBS, Dept Physiol, Lab Cardiovasc Physiol, Porto Alegre, RS - Brazil
[2] Univ Fed Rio Grande do Sul, ICBS, Dept Physiol, Lab Metab & Comparat Endocrinol, Porto Alegre, RS - Brazil
[3] Univ Fed Rio Grande do Sul, Escola Educ Fis, Lab Res Exercise, Porto Alegre, RS - Brazil
[4] Univ Sao Paulo, ICB, Dept Physiol & Biophys, BR-09500900 Sao Paulo - Brazil
[5] HC FMUSP, Inst Coracao, Hypertens Unit, Lab Expt Hypertens, Sao Paulo - Brazil
[6] Univ Fed Rio Grande do Sul, HCPA, Dept Internal Med, Div Endocrine, Porto Alegre, RS - Brazil
Total Affiliations: 6
Document type: Journal article
Source: FUNDAMENTAL & CLINICAL PHARMACOLOGY; v. 26, n. 6, p. 679-689, DEC 2012.
Web of Science Citations: 6
Abstract

Insulin and the inhibition of the reninangiotensin system have independent benefits for ischemiareperfusion injury, but their combination has not been tested. Our aim was to evaluate the effects of insulin+captopril on insulin/angiotensin signaling pathways and cardiac function in the isolated heart subjected to ischemiareperfusion. Isolated hearts were perfused (Langendorff technique) with KrebsHenseleit (KH) buffer for 25 min. Global ischemia was induced (20 min), followed by reperfusion (30 min) with KH (group KH), KH+angiotensin-I (group A), KH+angiotensin-I+captopril (group AC), KH+insulin (group I), KH+insulin+angiotensin-I (group IA), or KH+insulin+angiotensin-I+captopril (group IAC). Group A had a 24% reduction in developed pressure and an increase in end-diastolic pressure vs. baseline, effects that were reverted in groups AC, IA, and IAC. The phosphorylation of protein kinase B (AKT) was higher in groups I and IA vs. groups KH and A. The phosphorylation of AMP-activated protein kinase (AMPK) was similar to 31% higher in groups I, IA, and IAC vs. groups KH, A, and AC. The tert-butyl hydroperoxide (tBOOH)-induced chemiluminescence was lower (similar to 2.2 times) in all groups vs. group KH and was similar to 35% lower in group IA vs. group A. Superoxide dismutase content was lower in groups A, AC, and IAC vs. group KH. Catalase activity was similar to 28% lower in all groups (except group IA) vs. group KH. During reperfusion of the ischemic heart, insulin activates the AKT and AMPK pathways and inhibits the deleterious effects of angiotensin-I perfusion on SOD expression and cardiac function. The addition of captopril does not potentiate these effects. (AU)

FAPESP's process: 07/50554-1 - Glucose transporters and diabetes mellitus: contribution to the knowledge of glycemic control and chronic diseases development
Grantee:Ubiratan Fabres Machado
Support Opportunities: Research Projects - Thematic Grants