Artículos de revistas
Low-dose Enalapril Reduces Angiotensin II and Attenuates Diabetic-induced Cardiac and Autonomic Dysfunctions
Fecha
2012Registro en:
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, PHILADELPHIA, v. 59, n. 1, supl. 1, Part 1, pp. 58-65, JAN, 2012
0160-2446
10.1097/FJC.0b013e3182354776
Autor
Malfitano, Christiane
De Angelis, Katia
Fernandes, Tiago
Wichi, Rogerio Brandao
Rosa, Kaleizu
Pazzine, Mariana
Mostarda, Cristiano
Ronchi, Fernanda Aparecida
de Oliveira, Edilamar Menezes
Casarini, Dulce Elena
Irigoyen, Maria-Claudia
Institución
Resumen
Activation of renin-angiotensin system has been linked to cardiovascular and autonomic dysfunctions in diabetes. Experiments were performed to investigate the effects of angiotensin-converting enzyme inhibitor (ACEI), enalapril, on cardiac and autonomic functions in diabetic rats. Diabetes was induced by streptozotocin (50 mg/kg), and rats were treated with enalapril (1 mg.kg(-1).d(-1)). After 30 days, evaluations were performed in control, diabetic, and enalapril-treated groups. Cardiac function was evaluated by echocardiography and through cannulation of the left ventricle (at baseline and in response to volume overload). Heart rate and systolic blood pressure variabilities were evaluated in the time and frequency domains. Streptozotocin rats had left ventricular systolic and diastolic dysfunctions, expressed by reduced ejection fraction and increased isovolumic relaxation time. The ACEI prevented these changes, improved diastolic cardiac responses to volume overload and total power of heart rate variability, reduced the ACE1 activity and protein expression and cardiac angiotensin (Ang) II levels, and increased angiotensin-converting enzyme 2 activity, despite unchanged blood pressure. Correlations were obtained between Ang II content with systolic and diastolic functions and heart rate variability. These findings provide evidence that the low-dose ACEI prevents autonomic and cardiac dysfunctions induced by diabetes without changing blood pressure and associated with reduced cardiac Ang II and increased angiotensin-converting enzyme 2 activity.