title: Experimental induction of salt-sensitive hypertension is associated with lymphocyte proliferative response to HSP70.
abstract: 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.
authors.affiliation: Renal Service and Laboratory, Hospital Universitario and Universidad del Zulia, Maracaibo, Estado Zulia, Venezuela.
authors.forename: Gustavo
authors.initials: G
authors.lastname: Parra
authors.forename: Yasmir
authors.initials: Y
authors.lastname: Quiroz
authors.forename: Jenny
authors.initials: J
authors.lastname: Salazar
authors.forename: Yanauri
authors.initials: Y
authors.lastname: Bravo
authors.forename: Hector
authors.initials: H
authors.lastname: Pons
authors.forename: Maribel
authors.initials: M
authors.lastname: Chavez
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Johnson
authors.forename: Bernardo
authors.initials: B
authors.lastname: Rodriguez-Iturbe
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D015551:Autoimmunity / Q000502:physiology; D049109:Cell Proliferation / Q000187:drug effects*; D002478:Cells, Cultured; D004195:Disease Models, Animal; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism / Q000494:pharmacology*; D006973:Hypertension / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D007668:Kidney / Q000378:metabolism / Q000473:pathology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D011507:Proteinuria / Q000378:metabolism / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D055049:Salt Tolerance / Q000276:immunology / Q000502:physiology*; D013601:T-Lymphocytes / Q000187:drug effects / Q000473:pathology*
chemical_list: D018840:HSP70 Heat-Shock Proteins; D000804:Angiotensin II; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester