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Review
. 2012 Jan;39(1):96-103.
doi: 10.1111/j.1440-1681.2011.05482.x.

Renal inflammation, autoimmunity and salt-sensitive hypertension

Bernardo Rodríguez-Iturbe  1 , Martha Franco, Edilia Tapia, Yasmir Quiroz, Richard J Johnson
Affiliations
Review

Renal inflammation, autoimmunity and salt-sensitive hypertension

Bernardo Rodríguez-Iturbe et al. Clin Exp Pharmacol Physiol. 2012 Jan.

Abstract

1. The present article reviews the role of immune-competent cells infiltrating the kidney and their association with oxidative stress and renal angiotensin activity in the development of salt-sensitive hypertension. 2. We discuss changes in the pressure-natriuresis relationship resulting from renal inflammation and its improvement resulting from immunosuppressive treatment. 3. The potential role of T-cell-driven reactivity in sustaining the renal inflammation is examined in the light of accumulating evidence of autoimmune mechanisms in experimental and clinical hypertension.

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Conflict of interest statement

Disclosure: Dr Bernardo Rodriguez-Iturbe and Dr. Richard Johnson have a patent application with the University of Colorado on preventing or treating hypertension by inducing tolerance to HSP70. The other authors have no conflicts of interest.

Figures

Figure 1
Figure 1
Glomerular filtration rate (A), urinary sodium excretion (B) and fractional sodium excretion (C) in relation to renal artery pressure controlled by an aortic clamp at 90, 110, 130 mmHg in control rats (open crcles), in rats with salt-sensitive hypertension induced with transient inhibition of nitric oxide synthase with L-NAME) (SSHTN, closed squares) and in rats treated with L-NAME in whom suppression of inflammation was induced with the administration of mycophenolate mofetil (MMF, open squares). Impaired pressure natriuresis is evident in rats with inflammation-induced SSHTN that is partially corrected with MMF treatment. Methodology described in the text. Representative light microscopy (PAS staining × Original magnification ×200) of a biopsy of a rat in the SSHTN group (left side) showing tubulointerstitial inflammation and well-preserved glomerular structure. Tubulointerstitial inflammation is suppressed by MMF treatment (right side) *p<0.05 (two-tailed) vs. the rest (multigroup ANOVA, Tukey post-tests)
Figure 2
Figure 2
HSP70 overexpression is present in proximal tubular cells of rats with salt-sensitive hypertension induced by transient exposure to L-NAME (A) and absent in rats in which suppression of inflammation has been achieved with mofetil mycophenolate (B). (Immunoperoxidase staining, original magnification ×400)
Figure 3
Figure 3
Schematic representation of the pathogenesis of salt-sensitive hypertension. Mechanisms described in the text.
See this image and copyright information in PMC

References

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    1. Rodriguez-Iturbe B, Romero F, Johnson RJ. Pathophysiologic mechanisms of salt sensitive hypertension. Am J Kidney Dis. 2007;50:655–672. - PubMed
    1. Johnson RJ, Herrera J, Schreiner G, Rodríguez-Iturbe B. Acquired and subtle renal injury as a mechanism for salt-sensitive hypertension: Bridging the hypothesis of Goldblatt and Guyton. N Engl J Med. 2007;346:913–923. - PubMed
    1. Rodriguez-Iturbe B, Johnson RJ. The role of renal microvascular disease and interstitial inflammation in salt-sensitive hypertension. Hypertens Res. 2010;33:975–980. - PubMed
    1. Guyton AC. Blood pressure control: special role of the kidneys and body fluids. Science. 1991;252:1813–1816. - PubMed

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