Maternal high-sodium intake affects the offspring’ vascular renin-angiotensin system promoting endothelial dysfunction in rats

Santos-Rocha, Juliana; Lima-Leal, Geórgia A.; Moreira, Hicla S.; Ramos-Alves, Fernanda E.; Sá, Francine G. de; Duarte, Glória Pinto; Xavier, Fabiano E.

doi:10.1016/j.vph.2019.02.001

Cited by 6 publications

(4 citation statements)

References 42 publications

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“…It is well documented that the deleterious actions of angiotensin II in the vasculature, apart from its vasoconstrictor effect, occur through its significant pro-inflammatory property. This effect is due, at least in part, to the ability of angiotensin II to bind the AT 1 R receptor, upregulating inflammatory proteins, such as COX-2 [24,[54][55][56][57]. COX-2 is highly expressed in vessels of hypertensive patients or animal models where it participates in vascular dysfunction [54,[56][57][58][59], as well as in ouabain-treated animals [12,[30][31][32].…”

Section: Discussionmentioning

confidence: 99%

“…This effect is due, at least in part, to the ability of angiotensin II to bind the AT 1 R receptor, upregulating inflammatory proteins, such as COX-2 [24,[54][55][56][57]. COX-2 is highly expressed in vessels of hypertensive patients or animal models where it participates in vascular dysfunction [54,[56][57][58][59], as well as in ouabain-treated animals [12,[30][31][32]. Antioxidant, anti-inflammatory and anti-fibrotic effects of COX inhibition have been reported in several cardiovascular risk situations [23,24,56,58,[60][61][62].…”

Section: Discussionmentioning

confidence: 99%

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Cyclooxygenase-2 is a critical determinant of angiotensin II-induced vascular remodeling and stiffness in resistance arteries of ouabain-treated rats

França-Neto

Couto

Xavier

et al. 2022

Journal of Hypertension

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Objective: To investigate the role of angiotensin II/AT 1 receptor signaling and/or cyclooxygenase-2 (COX-2) activation on vascular remodeling and stiffening of the mesenteric resistance arteries (MRA) of ouabain-treated rats.Methods: Ouabain-treated (OUA, 30 mg kg/day for 5 weeks) and vehicle (VEH)-treated Wistar rats were cotreated with losartan (LOS, AT 1 R antagonist), nimesulide (NIM, COX-2 inhibitor) or hydralazine hydrochloride plus hydrochlorothiazide. MRA structure and mechanics were assessed with pressure myography and histology. Picrosirius red staining was used to determine the total collagen content. Western blotting was used to detect the expression of collagen I/III, MMP-2, Src, NFkB, Bax, Bcl-2 and COX-2. Reactive oxygen species (ROS) and plasma angiotensin II levels were measured by fluorescence and ELISA, respectively.Results: Blockade of AT 1 R or inhibition of COX-2 prevented ouabain-induced blood pressure elevation. Plasma angiotensin II level was higher in OUA than in VEH. LOS, but not hydralazine hydrochloride with hydrochlorothiazide, prevented inward hypotrophic remodeling, increased collagen deposition and stiffness, and oxidative stress in OUA MRA. LOS prevented the reduction in the total number of nuclei in the media layer and the Bcl-2 expression induced by OUA in MRA. The higher pSrc/Src ratio, NFkB/IkB ratio, and COX-2 expression in OUA MRA were also prevented by LOS. Likewise, COX-2 inhibition prevented vascular remodeling, mechanical changes, oxidative stress and inflammation in OUA MRA. Conclusion:The results suggest that, regardless of hemodynamic adjustments, the angiotensin II/AT 1 R/pSrc/ ROS/NFkB/COX-2 pathway is involved in the development of MRA inward hypotrophic remodeling and stiffness in ouabain-treated rats.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cyclooxygenase-2 is a critical determinant of angiotensin II-induced vascular remodeling and stiffness in resistance arteries of ouabain-treated rats

França-Neto

Couto

Xavier

et al. 2022

Journal of Hypertension

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“…Considering using cytokine for OA treatment, mesenchymal stem cell conditioned medium (MSC-CM) could be better choice for OA therapy (41). Therapeutic inhibition of AT1R or ACE can improve clinical symptoms by reducing the yield of in ammatory factors (16,17,19,20), delaying the development of OA. very few in vivo studies were published in this regard, which motivated our interests in examining concomitant use of MSCs-CM and RAS inhibitor drugs in an animal model of OA.…”

Section: Discussionmentioning

confidence: 99%

“…recent studies indicated the expression of major components of RAS, including ACE, AT1R, and AT2R in synovial tissue in humans and animals suggesting their probable engagement in the pathogenesis of OA and rheumatoid arthritis (RA); their expression is in accordance to the degree of in ammation and the severity of arthritis (10,(13)(14)(15). it has been shown that inhibition of AT1R or ACE could enhance clinical symptoms through suppression of in ammatory factors (16)(17)(18)(19)(20) delaying the progression of OA. captopril, an ACE inhibitor drug and Losartan (inhibitor of AT1R) has shown to have chondroprotective effect through suppression of local RAS in a rat model of osteoarthritis (21).…”

Section: Introductionmentioning

confidence: 99%

Induced Knee Osteoarthritis: Preventive Effects of Wharton-jelly Mesenchymal Stem Cell Conditioned Medium, Captopril and Losartan in Male Rats

Abolghasemi¹,

Tanideh

Alirezaee³

et al. 2023

Preprint

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Background: osteoarthritis (OA) is a degenerative joint disease that affect different parts of a synovial joint leading to pain and stiffness. Methods: forty male rats (220 ± 20 g, aged 10-12 weeks), were randomly divided into eight groups (n = 8). OA: anterior cruciate ligament transection (ACLT) + PBS. OA+ Hyaluronic acid (HA): ACLT+ treatment with HA. OA+ Captopril (Cap): ACLT + treatment with Cap. OA+ Losartan (Los): ACLT + treatment with Los. OA+ Wharton-jelly mesenchymal stem cell conditioned medium (WJ): ACLT + treatment with WJ OA+ WJ+ Cap.: ACLT + treatment with WJ. OA+ WJ+ Los.: ACLT + treatment with WJ and losartan Sham: No ACLT+ PBS. Osteoarthritis was induced through transection of the anterior cruciate ligament of both knees in rats. Three months after treatment, the samples were harvested and evaluated by histopathological, radiological and ACE activity analyses. Result:Histopathological and radiological findings indicated significant differences between the WJ+Cap and WJ+Los treated groups with OA+Cap OA+Los, the control and OA+HA groups (p ≤ 0:001). Significant differences were observed in the subchondral bone scores between WJ-CM+Cap, WJ+Los and WJ groups and OA+Cap, OA+Los, OA+HA groups (p ≤ 0:001). compared to WJ group alone, co-treatment of WJ and renin-angiotensin system (RAS) inhibitors (WJ+Cap and WJ+Los) showed better results regarding matrix scores (p ≤ 0:001). Conclusions: The group treated with WJ concomitant with RAS inhibitor drugs showed better outcomes than other groups in histopathological, radiological and angiotensin converting enzyme (ACE) activity evaluation.

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Maternal Nanomaterial Inhalation Exposure: Critical Gestational Period in the Uterine Microcirculation is Angiotensin II Dependent

et al. 2022

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Maternal high-sodium intake affects the offspring’ vascular renin-angiotensin system promoting endothelial dysfunction in rats

Cited by 6 publications

References 42 publications

Cyclooxygenase-2 is a critical determinant of angiotensin II-induced vascular remodeling and stiffness in resistance arteries of ouabain-treated rats

Cyclooxygenase-2 is a critical determinant of angiotensin II-induced vascular remodeling and stiffness in resistance arteries of ouabain-treated rats

Induced Knee Osteoarthritis: Preventive Effects of Wharton-jelly Mesenchymal Stem Cell Conditioned Medium, Captopril and Losartan in Male Rats

Maternal Nanomaterial Inhalation Exposure: Critical Gestational Period in the Uterine Microcirculation is Angiotensin II Dependent

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