| Autor: |
Ronchetti, Graziele Zandominegue, Simões, Maylla Ronacher, Schereider, Ingridy Reinholz Grafites, Leal, Marcos André Soares, Peçanha, Giulia Alessandra Wiggers, Padilha, Alessandra Simão, Vassallo, Dalton Valentim |
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| Zdroj: |
Cardiovascular Toxicology; Dec2022, Vol. 22 Issue 12, p929-939, 11p |
| Abstrakt: |
Mercury is considered a risk factor for the development of hypertension and other cardiovascular diseases. We investigated whether the effects of mercury exposure on haemodynamic parameters of young Wistar rats and prehypertensive SHRs might alter the time course of hypertension development. Young (4 weeks) male Wistar rats and SHRs were randomly assigned to four groups: untreated Wistar rats (Wistar Ct), Wistar rats exposed to mercury chloride for 30 days (Wistar Hg), untreated SHRs (SHR Ct) and SHRs exposed to mercury chloride (SHR Hg) for 30 days. Non-invasive and invasive arterial pressures were measured to investigate pressure reactivity; nitrite/nitrate levels, ACE activity, and lipid peroxidation were measured in plasma. The systolic blood pressure (SBP) of the Wistar rat groups did not change but increased in the SHRs from the second week to the last week. Hg exposure accelerated the increase in the SBP of SHRs. L-NAME administration increased SBP and diastolic blood pressure (DBP) in all groups, but this increase was smaller in SHRs exposed to Hg. A decrease in plasma nitrite and nitrate levels in the SHR Hg group suggested that mercury reduced NO bioavailability. Tempol-reduced blood pressure suggesting that the superoxide anion played a role in the marked increase in this parameter. These findings provide evidence that Hg exposure might activate mechanisms to accelerate hypertension development, including a reduction in NO bioavailability. Therefore, predisposed individuals under mercury exposure are at greater risk from an enhanced development of hypertension. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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