Effect of Exforge Hct and L-Arginine Treatments on Vascular Reactivity in Renovascular Hypertension
Name: IASMIM FERNANDES BARCELOS
Type: MSc dissertation
Publication date: 07/03/2018
Advisor:
Name |
Role |
|---|---|
| SONIA ALVES GOUVEA | Advisor * |
Examining board:
| Name |
Role |
|---|---|
| BRENO VALENTIM NOGUEIRA | Internal Alternate * |
| MARCELO PERIM BALDO | External Examiner * |
| MARCO CESAR CUNEGUNDES GUIMARÃES | Internal Examiner * |
| SONIA ALVES GOUVEA | Advisor * |
Summary: Diseases of the heart and vessels are the leading cause of death in Brazil. Renewascular hypertension is a major cause of secondary hypertension and is characterized by excessive activation of the renin angiotensin system. The objective of this study was to investigate the changes in mesenteric vascular reactivity induced by Exforge HCT and L-arginine in animals with 2R1C hypertension, as well as its effects on systolic blood pressure and target organ protection. Hypertension was induced by clipping the left renal artery (2R1C) and the rats were divided into groups: Sham, 2R1C, L-arginine, Exforge HCT and associated. After 21 days of treatment, all groups presented normalization of pressure levels. At the end of the experimental protocol, dose-response curves were performed on acetylcholine in resistance mesenteric arteries (Mulvany method). The nitric oxide pathway appears to be the major mechanism of vasodilation in the Sham, 2R1C and L-arginine groups, as observed in the acetylcholine dose-response curves following L-NAME and indomethacin blockades. In contrast, the Exforge HCT and associated groups presented their dose-response curves unchanged after double-blocking. Protein expression in samples from the mesenteric bed evaluated by Western blotting showed an increase of SOD-2 and gp91phox in all treated groups relative to the sham group. In conclusion, all treatments were able to improve vascular reactivity, restore blood pressure levels, reverse ventricular hypertrophy and improve vasodilator response in mesenteric arteries of rats with 2R1C arterial hypertension.
