Name: RAYNER ZANOTI PEREIRA

Publication date: 28/03/2024

Examining board:

Namesort descending Role
ANDRE SOARES LEOPOLDO Examinador Interno
PATRICK WANDER ENDLICH Examinador Externo
ROGER LYRIO DOS SANTOS Examinador Interno

Summary: Estrogen stimulates the production of nitric oxide (NO) and hydrogen sulfide (H2S), two potent
vasodilators. The decrease in ovarian hormones during postmenopause leads to vascular
tone deterioration, increasing the incidence of cardiovascular diseases (CVD) in women as a
result of this event. Physical exercise aids in improving the vasodilatory response of NO under
estrogen deficiency conditions, although the role of H2S remains uncertain. This study
investigated the effects of aerobic physical training on H2S formation in vascular reactivity in
the aorta of ovariectomized rats. Eight-week-old Wistar rats were randomly distributed into the
following groups: Sham + Sedentary (Sham + Sed); Sham + Exercise (Sham + Ex); OVX +
Sedentary (OVX + Sed); OVX + Exercise (OVX + Ex). After 7 days of ovariectomy and sham
surgery, the Ex group animals underwent a running physical training protocol. Initial and final
body mass, uterine mass, and visceral fat were recorded. The thoracic aorta was used to
evaluate vascular reactivity in a wire myograph. Nitric oxide (NO) and reactive oxygen species
(ROS) were quantified using 4,5-diaminofluorescein diacetate (DAF-2) and dihydroethidium
(DHE) probes, respectively. The results reveal an atrophic ovary after ovariectomy, indicating
deficiency of ovarian hormones. Physical training improved animal performance, reducing final
body mass and visceral fat. Sedentary groups showed decreased H2S-mediated vasodilation
compared to Ex animals. Sodium hydrosulfide (NaHS), an H2S donor, demonstrated similar
effects on vascular reactivity. Endothelium removal eliminated differences in dilation between
Sham and OVX groups and prevented physical training from enhancing H2S-mediated
vasodilatory response. Physical training increased NO formation and reduced ROS generation
in the thoracic aorta of Sham and OVX animals. Inhibition of nitric oxide synthase (NOS)
prevented training from improving H2S vasodilation in OVX animals while not affecting
relaxation in Sham animals. In conclusion, the absence of ovarian hormones compromises
the vasodilation capacity in aortic rings of ovariectomized rats. However, physical exercise
improves endothelium-dependent vasodilation involving H2S formation synergistically with NO
in the aorta of ovariectomized rats.

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