Oxidative stress, renal infiltration of immune cells, and salt-sensitive hypertension: all for one and one for all

Rodríguez‐Iturbe, Bernardo; Vaziri, Nosratola D.; Herrera-Acosta, Jaime; Johnson, Richard J.

doi:10.1152/ajprenal.00269.2003

Cited by 240 publications

(249 citation statements)

References 157 publications

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“…8 However, subsequent studies suggested that immune cell infiltration in the kidney may be the cause, not the result, of hypertension in this model. Indeed, in nearly all models of salt-sensitive hypertension, the tubulointerstitium of rat kidneys are infiltrated with lymphocytes and macrophages, 9,10 and a correlation between the intensity of the inflammatory cell infiltration and the severity of the blood pressure elevation was apparent. 11 In experimental models of hypertension, monocyte/macrophage infiltration of the perivascular fat renal tissue, as well as vascular adventitia, was observed.…”

Section: Experimental Data and Possible Pathways For Inflammation-indmentioning

confidence: 99%

Hypertension as an autoimmune and inflammatory disease

et al. 2016

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Section: Experimental Data and Possible Pathways For Inflammation-indmentioning

confidence: 99%

Hypertension as an autoimmune and inflammatory disease

et al. 2016

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“…We have raised the possibility that autoimmune reactivity could be responsible for the low-grade tubulointerstitial inflammation in the kidney that, in concert with local angiotensin II generation and oxidative stress, would provide the critical intrarenal milieu that would favor the chronic impairment in pressure natriuresis that underlies SSHTN. 74 Previous studies that examined the immune reactivity in hypertension have given conflicting results. In contrast with the experimental data that indicate that suppression of the immune system ameliorated hypertension, Tuttle and Boppana 75 reported that interleukin 2 had antihypertensive effects and it was suggested that activation of the immune system could be an adaptive response directed to suppress what otherwise could be life-threatening increments in blood pressure.…”

Section: Immune Reactivity and Hypertensionmentioning

confidence: 99%

The role of renal microvascular disease and interstitial inflammation in salt-sensitive hypertension

Rodríguez‐Iturbe¹,

Johnson

2010

Hypertens Res

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Primary (essential) hypertension has been shown to be mediated by a relative impairment in sodium excretion by the kidney, but the mechanisms responsible for this defect are still being clarified. Increasing evidence suggests a role for subtle acquired renal injury in mediating this process. Microvascular injury is present in the majority of subjects with hypertension. The development of arteriolosclerosis, primarily of the afferent arteriole, may interfere with glomerular autoregulation, whereas the loss of peritubular capillaries may facilitate local ischemia. These changes favor the localization of T cells and macrophages into the interstitium, which, coupled with local oxidative stress and angiotensin II generation, may contribute to the impaired pressure natriuresis observed with salt-sensitive hypertension. Consistent with this hypothesis, therapies that are aimed at blocking the immune response, including thymectomy, genetic alterations in mice resulting in impaired immune responses, or the use of immunosuppressive agents, can protect against the development of hypertension in experimental models. Preliminary data in humans also suggest that the inhibition of the renal inflammatory response may reduce blood pressure. The present investigations are directed to gain insight in the role of the intrarenal T-cell reactivity and autoimmunity in driving the tubulointerstitial inflammation and its participation in the pathogenesis of salt-sensitive hypertension.

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“…10,11 In the past decade, inflammation and oxidative stress have emerged as major players in vascular remodeling of hypertension in addition to known mechanisms, such as salt sensitivity, insulin resistance, and an imbalance in the renin-angiotensin system. 12 -15 Polymorphonuclear leukocytes (PMNL) are the main producer of reactive oxygen species (ROS) and have been shown to be involved in hypertension in both human and animal models.…”

Section: Essential Hypertension (Eh [Min1455]mentioning

confidence: 99%

An intronic variable number of tandem repeat polymorphisms of the cold-induced autoinflammatory syndrome 1 (CIAS1) gene modifies gene expression and is associated with essential hypertension

et al. 2006

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Cold-induced autoinflammatory syndrome 1 (CIAS1) gene is a member of the NALP subfamily of the CATERPILLER protein family that is expressed predominantly in peripheral blood leukocytes, which is to regulate apoptosis or inflammation through the activation of NF-jB and caspase. Recent genetic analyses suggested an association between inflammation and oxidative stress-related genes in the development of hypertension. This is the first genetic study indicating an association between the CIAS1 gene and susceptibility to essential hypertension (EH). The frequency of subject with the homozygote of 12 repeat allele was significantly higher in patients with hypertension compared with control subjects (987 cases, 924 controls) (P ¼ 0.030; odds ratio ¼ 1.24) at a novel VNTR polymorphism of CIAS1 intron 4 loci. We also found that the mean of systolic blood pressure of homozygotes of 12 repeat allele was 6.4 mmHg higher than those of homozygotes of non-12 repeat allele in male random population (P ¼ 0.009). The frequency of six SNPs spanning of the CIAS1 gene was not significantly between patients and controls. The real-time PCR analysis showed that among healthy young adults, 12-12 subjects expressed CIAS1 mRNA in peripheral leukocytes significantly more abundantly than homozygote of non-12 repeat alleles subjects (Po0.05). Reporter gene assay of the CIAS1-VNTR in HL60 stimulated by lipopolysaccharides showed that the intronic sequence involving 12 repeat increased the expression of luciferase compared with 9, 7, and 6 repeats.

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Oxidative stress, renal infiltration of immune cells, and salt-sensitive hypertension: all for one and one for all

Cited by 240 publications

References 157 publications

Hypertension as an autoimmune and inflammatory disease

Hypertension as an autoimmune and inflammatory disease

The role of renal microvascular disease and interstitial inflammation in salt-sensitive hypertension

An intronic variable number of tandem repeat polymorphisms of the cold-induced autoinflammatory syndrome 1 (CIAS1) gene modifies gene expression and is associated with essential hypertension

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