Name: OTAVIO LELIO DE JESUS DA SILVA
Publication date: 26/08/2022
Advisor:
Name |
Role |
|---|---|
| SONIA ALVES GOUVEA | Advisor * |
Examining board:
| Name |
Role |
|---|---|
| GLAUCIA RODRIGUES DE ABREU | Internal Examiner * |
| PATRICK WANDER ENDLICH | External Examiner * |
| SONIA ALVES GOUVEA | Advisor * |
Summary: Hypertension is the result of blood pressure disorders and can be caused by several factors such as sedentary lifestyle, poor diet and even insufficient hours of sleep. It is also related to kidney disease influenced by physiological factors, which are related to the renin-angiotensin-aldosterone process responsible for regulating blood water volume through sodium levels and also disorder in the sympathetic nervous system. The two-kidney, one-clip experimental model (2K1C) promotes renovascular hypertension, in addition to left ventricular hypertrophy, endothelial dysfunction, and increased levels of reactive oxygen species in the body (ROS), and ischemic heart disease. Treatments with angiotensin-converting enzyme (ACE) inhibitors and supplementation with precursors that potentiate NO synthesis may be one of the alternatives in the control of renovascular hypertension. Renovascular hypertension was induced in Wistar rats with a silver clip implanted in the left renal artery and the animals were divided into the following experimental groups: SHAM, 2-kidneys, 1-clip (2K1C), 2K1C treated with benazepril (BEN), 2K1C treated with L-arginine (L-ARG) and 2K1C treated with an association of Benazepril+L-arginine (Association), treatments started 7 days after clipping and lasted for 3 consecutive weeks. Blood pressure was measured at the beginning, seven days after clipping and at the end of the treatment (28º). After 21 days of treatment, only the BEN+L-ARG group was effective in normalizing systolic blood pressure when compared to the 2K1C and SHAM groups. Our findings also show that the treatments were effective in improving blood pressure in rats with renovascular hypertension. The antioxidant effect of benazepril and its ability to reduce oxidative stress and the supply of NO by L-arginine may be an important mechanism for the improvement in vascular remodeling found in our studies. Therefore, our work demonstrates that treatment with BEN associated with L-arginine was effective in reducing BP and preventing hypertrophy, in addition, we point out that the mechanisms involved in these effects seem to be related to a reduction in oxidative stress in the increase of NO bioavailability.
