Development of renal atrophy in murine 2 kidney 1 clip hypertension is strain independent

Kashyap, Sonu; Boyilla, Rajendra; Zaia, Paula J.; Ghossan, Roba; Nath, Karl A.; Textor, Stephen C.; Lerman, Lilach O.; Grande, Joseph P.

doi:10.1016/j.rvsc.2016.06.002

Cited by 6 publications

(4 citation statements)

References 36 publications

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“…However, the restoration of the antioxidant enzyme activities with the marked reduction in LPO in the kidneys of hypertensive rats treated with taurine indicates it beneficial antioxidant role in the treated rats. The renal histological alterations observed in the presents study corroborate earlier studies on hypertensioninduced renal damage in rats [61][62]. The histopathological damage identified in kidneys of L-NAME-induced hypertensive rats includes congestion of blood vessels, hemorrhagic lesion and disorganized glomerular structure.…”

Section: Discussionsupporting

confidence: 88%

Taurine Ameliorates Thyroid Hypofunction and Renal Injury in L-NAME-Induced Hypertensive Rats

et al. 2018

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There is a growing global interest in hypertension due to its associated complications including renal dysfunction in patients. The thyroid system reportedly regulates renal function in both animal and human. The present study investigated the therapeutic efficacy of taurine on renal and thyroid dysfunctions in hypertensive rats. Hypertension was induced by oral administration of nitric oxide synthase inhibitor, N-nitro L-arginine-methyl-ester (L-NAME), at 40 mg/kg body weight to the male Wistar rats for 14 consecutive days. The hypertensive rats were subsequently treated with either taurine (100 and 200 mg/kg) or reference drug atenolol (10 mg/kg) for another 14 consecutive days. Hypertensive rats showed renal damage evidenced by elevated plasma creatinine and urea levels when compared with normotensive control rats. Furthermore, L-NAME-induced hypertensive rats showed decreased circulatory concentrations of thyroid stimulating hormone, thyroxine, triiodothyronine and the ratio of triiodothyronine to thyroxine. The marked decrease in the renal antioxidant enzyme activities and nitric oxide level was accompanied by significant increase in myeloperoxidase activity and biomarkers of oxidative stress in hypertensive rats. Histological examination of kidneys from hypertensive rats revealed congestion of blood vessels, hemorrhagic lesion and disorganized glomerular structure. However, treatment with taurine or atenolol significantly reversed the suppression of thyroid function, ameliorated renal oxidative stress and histopathological lesions in L-NAME-induced hypertensive rats. Taurine may be a useful chemotherapeutic supplement in enhancing renal and thyroid functions in hypertensive patients.

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Section: Discussionsupporting

confidence: 88%

Taurine Ameliorates Thyroid Hypofunction and Renal Injury in L-NAME-Induced Hypertensive Rats

et al. 2018

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“…RAS caused hypertension and progressive loss of stenotic kidney volume (Figs 2A–C , S5A ) 24 . Flow cytometric analysis showed increased numbers of total CD11b + F4/80 + macrophages and complementary DC (cDC1) in the stenotic kidney after 4 weeks of RAS (Fig.…”

Section: Resultsmentioning

confidence: 98%

Kidney-resident macrophages promote a proangiogenic environment in the normal and chronically ischemic mouse kidney

Puranik

Leaf

Jensen

et al. 2018

Sci Rep

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Renal artery stenosis (RAS) caused by narrowing of arteries is characterized by microvascular damage. Macrophages are implicated in repair and injury, but the specific populations responsible for these divergent roles have not been identified. Here, we characterized murine kidney F4/80+CD64+ macrophages in three transcriptionally unique populations. Using fate-mapping and parabiosis studies, we demonstrate that CD11b/cint are long-lived kidney-resident (KRM) while CD11chiMϕ, CD11cloMϕ are monocyte-derived macrophages. In a murine model of RAS, KRM self-renewed, while CD11chiMϕ and CD11cloMϕ increased significantly, which was associated with loss of peritubular capillaries. Replacing the native KRM with monocyte-derived KRM using liposomal clodronate and bone marrow transplantation followed by RAS, amplified loss of peritubular capillaries. To further elucidate the nature of interactions between KRM and peritubular endothelial cells, we performed RNA-sequencing on flow-sorted macrophages from Sham and RAS kidneys. KRM showed a prominent activation pattern in RAS with significant enrichment in reparative pathways, like angiogenesis and wound healing. In culture, KRM increased proliferation of renal peritubular endothelial cells implying direct pro-angiogenic properties. Human homologs of KRM identified as CD11bintCD11cintCD68+ increased in post-stenotic kidney biopsies from RAS patients compared to healthy human kidneys, and inversely correlated to kidney function. Thus, KRM may play protective roles in stenotic kidney injury through expansion and upregulation of pro-angiogenic pathways.

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“…2K1C hypertension was produced with methods described previously ( 26 , 41 , 59 ). Mice were anesthetized with isoflurane (2–3% in 100% oxygen).…”

Section: Methodsmentioning

confidence: 99%

Excessive dietary salt promotes aortic stiffness in murine renovascular hypertension

DeLalio

Hahn

Katayama

et al. 2020

American Journal of Physiology-Heart and Circulatory Physiology

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Renal artery stenosis is the most common cause of secondary hypertension. The 2‐kidney‐1‐clip (2K1C) model of renal stenosis is associated with elevated arterial blood pressure (ABP), activation of the sympathetic nervous system, and blunted reno‐renal reflexes and natriuretic responses. Excess dietary salt intake has multiple actions on the cardiovascular system and exacerbates ABP in some models of hypertension. The present study tested the hypothesis that 2K1C mice exhibit salt sensitive hypertension and worsening cardiovascular responses to high salt feeding. Male C57Bl6 mice (8–12 weeks) were fed 0.1% NaCl or 4% NaCl diets and ABP was continuously monitored using telemetry. 2K1C hypertension was produced by placing a 0.5mm length of PTFE tubing around the right renal artery. Baseline 24‐h mean ABP was not different between 0.1% versus 4.0% NaCl fed mice (101±1 vs 99±1 mmHg, respectively; n=8/group). 2K1C significantly increased ABP in both groups; however, 24‐h mean ABP at 3 weeks post‐renal clipping was not different between mice fed 0.1% vs 4.0% NaCl (122±3 vs. 124±6 mmHg, respectively; n=8/group). In addition, renal artery stenosis significantly increased arterial pulse pressure (systolic‐diastolic) in 0.1% NaCl (Day 0: 35±1 vs Day 21: 42±1 mmHg, P<0.05) and 4.0% NaCl (Day 0: 36±1 vs Day 21: 49±3 mmHg, P<0.05). Interestingly, the magnitude of the increase in arterial pulse pressure was significantly greater in mice fed 4.0% vs 0.1% NaCl (Δ14±3 vs Δ7±2 mmHg, P<0.05). This suggests dietary salt intake promotes aortic stiffness in the 2K1C model. To test this, endothelial‐dependent vasodilatory responses were measured using myography in sham and 2K1C mice fed 0.1% and 4.0% NaCl diets for 3 weeks. 4.0% NaCl 2K1C mice exhibited significantly blunted aortic vasodilation responses versus 2K1C mice fed 0.1% NaCl or sham mice fed 0.1% or 4.0% NaCl. These effects were not observed in the mesenteric arteries of the same animal. In vivo, pulse wave velocity (PWV) measurements revealed a significantly higher PWV value in 2K1C mice fed 4.0% NaCl versus 2K1C fed 0.1% NaCl (3.97±0.19; n=7 vs. 3.18±0.19; n=8, P<0.01) or sham fed 0.1% or 4.0% NaCl (3.21±0.19; n=7 vs. 3.01±0.19; n=7). We conclude that high dietary salt does not exaggerate the chronic hypertension in 2K1C mice but produces a specific endothelial‐dependent aortic stiffness. Support or Funding Information RO1 HL128388 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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Development of renal atrophy in murine 2 kidney 1 clip hypertension is strain independent

Cited by 6 publications

References 36 publications

Taurine Ameliorates Thyroid Hypofunction and Renal Injury in L-NAME-Induced Hypertensive Rats

Taurine Ameliorates Thyroid Hypofunction and Renal Injury in L-NAME-Induced Hypertensive Rats

Kidney-resident macrophages promote a proangiogenic environment in the normal and chronically ischemic mouse kidney

Excessive dietary salt promotes aortic stiffness in murine renovascular hypertension

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