Chronic Mercury Exposure in Prehypertensive SHRs Accelerates Hypertension Development and Activates Vasoprotective Mechanisms by Increasing NO and H2O2 Production

Fardin, P; Simões, Rakel Passos; Schereider, Ingridy Reinholz Grafites; Almenara, Camila Cruz Pereira; Vassallo, Dalton Valentim

doi:10.1007/s12012-019-09545-6

Cited by 8 publications

(8 citation statements)

References 62 publications

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“…In fact, recently we showed that mercury exposure could accelerated the hypertension development of young SHR. 26,27 However, this effect was accompanied by a vasoprotective mechanism, which includes an increase of NO, against the early establishment of hypertension in resistance arteries of young SHR. Therefore, we evaluated the effect of mercury exposure in in vivo young SHR to elucidate how this metal changes blood pressure at the same time that vasoprotective mechanisms were occurring, as observed previously.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, we evaluated the effect of mercury exposure in in vivo young SHR to elucidate how this metal changes blood pressure at the same time that vasoprotective mechanisms were occurring, as observed previously. 27 Thus, we evaluated mercury effects by recording invasive and noninvasive arterial blood pressure. Our results showed an accelerated increase of the SBP (noninvasive recordings) in young SHR exposed to mercury chloride from the second week of treatment.…”

Section: Discussionmentioning

confidence: 99%

“…It is well established that Hg activates NADPHoxidase and COX consequently increasing free radicals production and producing vasoconstriction. 13,25,26,27 NO can react with the superoxide anion forming peroxynitrite, another vasoconstrictor. 45 So, we evaluated the involvement of superoxide anion and oxidative stress in animals exposed to Hg.…”

Section: Discussionmentioning

confidence: 99%

“…23 Previously, we demonstrated that mercury exposure for 30 days accelerates the development of hypertension in young SHR animals. 26,27 However, the systemic mechanisms by which this metal induces the early development of hypertension in these animals has not yet been described. As mentioned above, mercury exposure induces an increase ACE activation at vascular level that enhances oxidative stress reducing NO bioavbailability.…”

Section: Introductionmentioning

confidence: 99%

“…As mentioned above, mercury exposure induces an increase ACE activation at vascular level that enhances oxidative stress reducing NO bioavbailability. 22,25,26,27 On the other hand, the systemic renin-angiotensin system (RAS) plays a role for hypertension development, especially in SHR. Therefore, we hypothetized that low-mercury exposure could accelerate the increment of blood pressure in SHR animals by a systemic mechanism that involves increase of renin-angiotensin system activity and reduction of NO bioavailability.…”

Section: Introductionmentioning

confidence: 99%

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Oxidative stress-induced by 30 days of mercury exposure triggers acceleration of hypertension development in prehypertensive young SHR rats

Ronchetti

Schereider

Leal

et al. 2022

Preprint

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Mercury is considered a risk factor for hypertension development and other cardiovascular diseases. Objectives: We investigated whether the effects of mercury exposure on hemodynamic parameters of young Wistar and prehypertensive SHR animals might influence the time course of hypertension development. Main methods: Young (4 weeks) male Wistar and SHR rats were randomly assigned to 4 groups: untreated Wistar rats (Wistar Ct), Wistar rats exposed to mercury chloride (Wistar Hg); untreated SHR rats (SHR Ct) and SHR rats exposed to mercury chloride (SHR Hg) for 30 days. Non-invasive and invasive arterial pressure were measured to investigate pressure reactivity; nitrite/nitrate levels, ACE activity, and lipid peroxidation were measured in plasma. Results: Systolic blood pressure (SBP) of Wistar groups did not change but increased in SHR from the second week to the last one. Hg exposure accelerated the increase of SBP in SHR rats. L-NAME administration increased SBP and diastolic blood pressure (DBP) in all groups, but this increase was smaller in SHR animals exposed to Hg. A decrease of plasma nitrite and nitrate in 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 of this parameter. These findings provide evidence that the effects of exposure to Hg might trigger mechanisms to accelerate the hypertension development including NO bioavailability reduction. Therefore, mercury might enhance the risk to cardiovascular disorders not only for adults but also for pre-disposed young ones enhancing hypertension development.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%