Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 51-year-old woman who had been treated for years for rheumatoid arthritis presented with a persistent dry cough and shortness of breath three weeks after administration of the ACE inhibitor temocapril hydrochloride against essential hypertension. Chest radiography and computed tomography showed diffuse reticular shadows and ground-grass opacities in both lung fields. Bronchoalveolar lavage fluid analysis showed an increase of lymphocytes and CD8+ T cells (93.3% of lymphocytes), and a decrease of the CD4/8 ratio of the T cell subset (0.04). Histopathological analysis of trans-bronchial lung biopsy specimens showed infiltration of lymphocytes into the alveolar septa and exudation of alveolar macrophages, signs characteristic of interstitial pneumonia. A drug lymphocyte stimulation test was positive for temocapril, but negative for other drugs. On the basis of these findings, we diagnosed temocapril hydrochloride-induced interstitial pneumonia.
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PMID:[A case of interstitial pneumonia induced by an ACE inhibitor (temocapril hydrochloride)]. 1453 3

Hypertension affects one-third of the adult population of the world. The causes of hypertension are incompletely understood, but relative impairment of sodium excretion is central to its pathogenesis. Immune cell infiltration in the kidney is a constant finding in hypertension that in association with local angiotensin and oxidants causes a defect in sodium excretion. However, it is unclear if the T cell influx into the kidney responds to nonspecific chemokine cues or is due to antigen-driven immune attraction. We found that T cells in experimentally induced salt-driven hypertension present a CD4 clonal response to heat shock protein 70 (HSP70) that is overexpressed in the kidney. We used a highly preserved amino acid sequence within the HSP molecule to induce immune tolerance associated with the generation of IL-10 producing regulatory T cells. Immune tolerant rats to HSP70 developed minimal renal inflammation and were protected from the development of salt-sensitive hypertension. Adoptive transfer of T lymphocytes isolated from spleen of tolerized rats also reversed hypertension. HSP70 gene delivery to the renal vein of the kidneys of rats sensitized to HSP70 caused an increment in blood pressure in response to a high-salt diet. The HSP70 peptide used in this work induces a strong proliferative response in peripheral blood lymphocytes of patients with essential hypertension. These studies provide evidence that autoimmunity plays a role in salt-sensitive hypertension and identifies HSP70 expressed in the kidney as one key antigen. These findings raise the possibility of novel approaches to the treatment of this condition.
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PMID:Immune reactivity to heat shock protein 70 expressed in the kidney is cause of salt-sensitive hypertension. 2309 71