Experimental induction of salt-sensitive hypertension is associated with lymphocyte proliferative response to HSP70

Gustavo Parra, Yasmir Quiroz, Jenny Salazar, Yanauri Bravo, Hector Pons, Maribel Chavez, Richard J. Johnson, Bernardo Rodriguez-Iturbe

Research output: Articles / NotesScientific Articlepeer-review

27 Scopus citations


Renal tubulointerstitial inflammation is a constant feature of experimental models of hypertension and likely plays a role in the pathogenesis of salt-sensitive hypertension. We have previously raised the possibility that the immune cell infiltration is driven by a low grade autoimmune reactivity directed to or facilitated by renal heat shock protein over expression. The present studies were done to gain insight on possible cell-mediated immune mechanisms in experimental hypertension by determining the renal expression of HSP70 and the proliferation index of T lymphocytes cultured with HSP70. We studied male Sprague-Dawley rats with inhibition of nitric oxide (NO) synthase (n=6), protein overload (PO) proteinuria (n=7) and short-term angiotensin II (Ang II) infusion (n=5), and their corresponding control groups. Each model was associated with 2 to 4 fold increase (P<0.05-0.001) in renal HSP70 expression. T cells isolated from the spleens demonstrated a significant two- to nine-fold response compared to controls (P<0.05 or lower for each comparison) when cultured with HSP70. These studies suggest that autoimmunity to stress proteins is involved in the sustained low-grade inflammatory infiltration that occurs in the tubulointerstitial areas of the hypertensive kidney.

Original languageEnglish
Pages (from-to)S55-S59
JournalKidney International
Issue numberSUPPL. 111
StatePublished - Dec 2008
Externally publishedYes


  • Autoimmunity
  • Heat shock proteins
  • Lymphocytes
  • Renal tubulointerstitium
  • Salt-dependent hypertension


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