Impaired pressure natriuresis is associated with interstitial inflammation in salt-sensitive hypertension

Rodríguez‐Iturbe, Bernardo; Franco, Martha; Johnson, Richard J.

doi:10.1097/mnh.0b013e32835b3d54

Cited by 23 publications

(17 citation statements)

References 69 publications

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“…The role played by oxidative stress in the medullary regions of the kidney, restricting nitric oxide availability and causing dysfunction of the pressure-natriuresis response, has been reviewed recently (8,30,36,48). Reduction of oxidative stress by hypoxiainducible factor 1␣ (23) can improve pressure natriuresis.…”

Section: Discussionmentioning

confidence: 99%

“…Pressure natriuresis refers to the increment in urinary sodium excretion (U Na V) that occurs when blood pressure rises and is the consequence of complex modifications in renal interstitial hydrostatic pressure, medullary blood flow, nitric oxide, reactive oxygen species, prostaglandins, and angiotensin II activity (8,30,36) that result in coordinated decreases in the surface distribution of apical sodium-hydrogen exchangers and basolateral Na-K ATPase activity (27). In SSHTN, the pressure-natriuresis relationship is less steep and shifted to the right so that higher bloodpressure levels are necessary to drive the natriuretic response required to maintain sodium balance (41).…”

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Impaired pressure natriuresis resulting in salt-sensitive hypertension is caused by tubulointerstitial immune cell infiltration in the kidney

Franco

Tapia

Bautista

et al. 2013

American Journal of Physiology-Renal Physiology

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-Iturbe B. Impaired pressure natriuresis resulting in salt-sensitive hypertension is caused by tubulointerstitial immune cell infiltration in the kidney. Am J Physiol Renal Physiol 304: F982-F990, 2013. First published January 30, 2013 doi:10.1152/ajprenal.00463.2012.-Immune cell infiltration of the kidney is a constant feature in salt-sensitive hypertension (SSHTN). We evaluated the relationship between the renal inflammation and pressure natriuresis in the model of SSHTN that results from transient oral administration of N -nitro-L-arginine methyl ester (L-NAME). Pressure natriuresis was determined in Wistar rats that received 4 wk of a high-salt (4% NaCl) diet, starting 1 wk after stopping L-NAME, which was administered alone (SSHTN group, n ϭ 17) or in association with mycophenolate mofetil (MMF; MMF group, n ϭ 15). The administration of MMF in association with L-NAME is known to prevent the subsequent development of SSHTN. Control groups received a high (n ϭ 12)-and normal (0.4%)-salt diet (n ϭ 20). Rats with SSHTN had increased expression of inflammatory cytokines and oxidative stress. The severity of hypertension correlated directly (P Ͻ 0.0001) with the number of tubulointerstitial immune cells and angiotensin II-expressing cells. Pressure natriuresis was studied at renal arterial pressures (RAPs) of 90, 110, 130, and 150 mmHg. Glomerular filtration rate was similar and stable in all groups, and renal blood flow was decreased in the SSHTN group. Significantly decreased natriuresis (P Ͻ 0.05) was found in the SSHTN group at RAPs of 130 and 150 mmHg, and there was an inverse correlation (P Ͻ 0.01) between the urinary sodium excretion and the number of tubulointerstitial inflammatory cells (lymphocytes and macrophages) and cells expressing angiotensin II. We conclude that tubulointerstitial inflammation plays a key role in the impairment of pressure natriuresis that results in salt-dependent hypertension in this experimental model. angiotensin II-positive cells; lymphocytes; macrophages; mycophenolate mofetil; urinary sodium excretion ARTERIAL HYPERTENSION IS A major cause of morbidity and mortality worldwide. Salt sensitivity, characterized by greater-thanexpected blood-pressure changes in response to salt loading and restriction, is a feature of the majority of adult and elderly hypertensive patients (53) and is associated with renal tubulointerstitial inflammation in experimental models of hypertension (37, 38) and in primary hypertension in humans (11,14,49). The relevance of the renal inflammation in the pathogenesis of saltsensitive hypertension (SSHTN) is underlined by the demonstration that treatments that suppress the renal inflammation result in amelioration or prevention of salt-driven hypertension (11,38,51).It is assumed that the role played by renal inflammation is related to the impairment in the renal capacity to excrete sodium, since the central event in the pathogenesis of salt-induced hypertension is impairment in the pressure-natriuresis relationship (9). Pressure natriuresis refers to...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Impaired pressure natriuresis resulting in salt-sensitive hypertension is caused by tubulointerstitial immune cell infiltration in the kidney

Franco

Tapia

Bautista

et al. 2013

American Journal of Physiology-Renal Physiology

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“…Details of the mechanisms by which renal interstitial inflammation may cause hypertension have been recently reviewed elsewhere. 15 Evidence showing the effects of renal interstitial inflammation also comes from experimental studies that investigated the impact of anti-inflammatory cytokines, such as IL-10, on blood pressure. Tinsley et al 16 showed that the administration of intraperitoneal IL-10 normalized blood pressure and improved endothelial dysfunction in pregnant deoxycorticosterone acetate/saline-treated rats.…”

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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“…Although angiotensinogen is the best understood example, reports indicate that, at least in rodents, ACE and tubular renin expression are also upregulated in many conditions associated with renal parenchymal injury. Another suggestion is that inflammatory cells express RAS components and therefore, in conditions of renal inflammation, can become a separate source of local angiotensin II [28, 29]. …”

Section: Introductionmentioning

confidence: 99%

Renal Generation of Angiotensin II and the Pathogenesis of Hypertension

et al. 2014

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The existence of a complete and functional renin-angiotensin system along the nephron is widely recognized. However, its precise role in blood pressure control and, by extension, hypertension is still uncertain. While most investigators agree that overexpressing RAS components along the nephron results in hypertension, two important issues remain: whether the local RAS works as a separate entity or represents an extension of the systemic RAS and whether locally generated angiotensin II has specific renal effects on blood pressure that are distinct from systemic angiotensin II. This review addresses these issues while emphasizing the unique role of local angiotensin II in the response of the kidney to hypertensive stimuli and the induction of hypertension.

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Impaired pressure natriuresis is associated with interstitial inflammation in salt-sensitive hypertension

Abstract: Here, we review the mechanisms for the impairment in pressure natriuresis resulting from renal tubulointerstitial inflammation in reference to the normal physiologic mechanisms involved in this response.

Cited by 23 publications

References 69 publications

Impaired pressure natriuresis resulting in salt-sensitive hypertension is caused by tubulointerstitial immune cell infiltration in the kidney

Impaired pressure natriuresis resulting in salt-sensitive hypertension is caused by tubulointerstitial immune cell infiltration in the kidney

Hypertension as an autoimmune and inflammatory disease

Renal Generation of Angiotensin II and the Pathogenesis of Hypertension

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