Endothelin in the progressive renal disease of glomerulopathies

Research output: Contribution to journalArticlepeer-review

Abstract

Endothelin (ET) isopeptides are synthetized in the kidney and act as local hormones with an impressive number of diverse autocrine and paracrine functions. A variety of proinflammatory and vasoactive agents including thrombin, transforming growth factor β, angiotensin II as well as mechanical forces enhance the renal synthesis of ET. Two receptor subtypes, ETA and ET(B), are widely expressed in the kidney, coupled to multiple intracellular signal transduction pathways that mediate distinct activities. Renal vessels are peculiarly sensitive to the vasoconstrictive effect of ET, which, infused in the kidney, decreases renal blood flow and glomerular filtration rate. This effect, together with the capability of ET to induce contraction and proliferation of mesangial cells, as well as accumulation of mesangial matrix proteins, have suggested that ET may participate in the renal events that lead to renal disease progression. Evidence is now available that renal ET does play a role in the process of progressive renal injury in chronic models of renal disease to the extent that the selective pharmacological manipulation of ET pathway has a major positive impact on the progression of the disease. By contrast, more work is necessary to define the role of ET in the pathophysiology of human glomerulopathy. The recent availability of orally active compounds with potential human use, may hopefully speed progress in the area.

Original languageEnglish
Pages (from-to)283-291
Number of pages9
JournalMineral and Electrolyte Metabolism
Volume21
Issue number4-5
Publication statusPublished - 1995

Keywords

  • Cyclosporine nephrotoxicity
  • Diabetes
  • Endothelin
  • Endothelin receptors
  • Renal disease progression
  • Ureteral obstruction
  • Urinary endothelin

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

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