Functional studies in small arteries do not support a primary role for endothelin in the pathogenesis of Raynaud's disease

PJW Smith, CJ Ferro, DS McQueen, DJ Webb*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Endothelin-1 (ET-1) has been implicated in the pathogenesis of Raynaud's disease (RD). This study examined the effect of cooling on the response to ET-1 in human microvessels. Subcutaneous small arteries were dissected from gluteal fat biopsies taken from patients with RD (n = 20) and from age- and sex-matched control subjects (n = 17) and were cannulated in a small vessel arteriograph. Cumulative concentration-response curves to ET-1 (10(-12) to 3 x 10(-7) M were obtained in vessels at 37degreesC and 24degreesC, with the endothelium either intact or removed (n = 6 per group). There were no significant differences in responses to ET-1 between RD patients and controls in either intact or denuded vessels, at either 37degreesC or at 24degreesC. There was, however, a significant endothehum-dependent interaction between the groups when the effect of temperature on the response to ET-1 was examined (p = 0.01; two-way ANOVA). Whereas cooling tended to reduce the sensitivity in RD, the opposite effect was observed in controls. Measurements of plasma ET-1 did not reveal any significant difference between patients with RD and healthy controls. These results suggest that ET-1 does not play a primary pathophysiologic role in RD. ET-1 might be responsible for mediating the prolonged vasospasm in RD, but secondary to another factor(s), such as impaired endothelium-dependent vasodilatation.

Original languageEnglish
Pages (from-to)S473-S476
Number of pages4
JournalJournal of cardiovascular pharmacology
Volume31
DOIs
Publication statusPublished - 1998

Keywords

  • Raynaud's disease
  • endothelium
  • endothelin
  • cooling
  • small arteries
  • human

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