Name: RAKEL PASSOS SIMÕES
Publication date: 24/06/2019
Advisor:
Name |
Role |
|---|---|
| ALESSANDRA SIMAO PADILHA | Advisor * |
Examining board:
| Name |
Role |
|---|---|
| ALESSANDRA SIMAO PADILHA | Advisor * |
| DALTON VALENTIM VASSALLO | Co advisor * |
| FABIANA DAYSE MAGALHAES SIMAN MEIRA | External Examiner * |
| JONAINA FIORIM PEREIRA DE OLIVEIRA | External Examiner * |
| LEONARDO DOS SANTOS | Internal Examiner * |
Summary: Mercury is a heavy metal widely dispersed in nature and upon contact with the human body causes damage to the vessels and to the heart, promoting the development of cardiovascular diseases. Chronic exposure to mercury chloride (HgCl2) for 30 daysdoes not change blood pressure in adult normotensive rats, however,it is unknown
what would be the effects of this exposure on prehypertensive animals. Thus, we aimed to compare the effects of chronic exposure to HgCl2 in normotensive rats and young spontaneously hypertensive rats (SHR). Four-week-old Wistar and SHR were treated daily with HgCl2(1st dose 4.6 μg/kg, subsequent dose 0.07μg/kg/day, im, 30days) or 0.9% saline.
In young normotensive animals, mercury exposure did not change systolic blood pressure (SBP), vascular reactivity to phenylephrine, superoxide anion production and the COX-2 pathway. However, it abolished modulation of contraction of aortic rings by the prostacyclin receptor (IP). In SHR, exposure to HgCl2 accelerated the development
of hypertension and increased vascular reactivity to phenylephrine, at least in part, by increasing the participation of the EP1 pathway and reducing IP pathway. In addition, HgCl2 increased oxidative stress, confirmed by higher in situproduction of superoxide anion, and reduced the participation of antioxidant enzymes, corroborated with the decrease in SOD-1 protein levels in aorta. Together, these effects
characterize endothelial dysfunction in SHR and this seems to be the reason why mercury accelerates the development of hypertension in these animals. These findings suggest that mercury exposure changes
the natural course of hypertension in young SHR and is a cardiovascular risk factor for pre-hypertensive individuals
