Name: KAROLINE ALVES ROSSI

Publication date: 03/06/2022
Advisor:

Namesort descending Role
ALESSANDRA SIMAO PADILHA Advisor *

Examining board:

Namesort descending Role
ALESSANDRA SIMAO PADILHA Advisor *
FABIANA DAYSE MAGALHAES SIMAN MEIRA External Examiner *
SILVANA DOS SANTOS MEYRELLES Internal Examiner *

Summary: Studies have shown that Cadmium exposure is associated with important vascular
changes, often related to increased blood pressure. However, it is not known whether
the effects of exposure to low concentrations for a short period could promote vascular
dysfunction, and what are the mechanisms involved in this process. The aim of this
study was to describe the pressoric and vascular effects of 7-day exposure to ClCd2
in rats. For this, Wistar rats received drinking water (Ct) or 100 mg/L ClCd2 solution
(Cd) via drinking water for 7 days. Weight, plasma cadmium concentration, systolic
blood pressure (SBP) and aortic ring responses to vasoactive agents were analyzed.
Even at low plasma concentration (1.66 ± 0.38 μg/L), the animals exposed to the metal
showed an increase in SBP (141.5 ± 3.0 vs 128.7 ± 1.84 mmHg) and in the contractile
response to Phenylephrine (Phe). Removal of vascular endothelium and inhibition of
the enzyme nitric oxide synthase (NOS) through L-NAME (100 μM) similarly increased
contraction to Phenylephrine. Despite this, there was an increase in the protein
expression of peNOS Ser1177 and in the basal production of nitric oxide (NO). Removal
of H2O2 through Catalase incubation (1000 U/ml-1) reduced the contractile response
only in the Cd group, which showed lower expression of Catalase and increased basal
production of H2O2. In Phe (1 μM) pre-contracted rings, Cd group showed a reduction
in endothelium-dependent (ACh) and independent (SNP) relaxation when compared
to Ct group. However, in KCl (60 mM) pre-contracted rings, the response to SNP was
similar between groups. Together, the results demonstrate that 7 days of exposure to
Cadmium lead to increased blood pressure and aortic contraction to Phe and reduced
relaxation. These vascular effects seem to involve reduced Catalase antioxidant
defense against H2O2, with reduced activation of potassium channels, balanced by an
increase in eNOS activity.

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