Mineralocorticoids upregulate arterial contraction to epidermal growth factor

Jennifer A. Florian, Anne Dorrance, R. Clinton Webb, Stephanie W. Watts

Research output: Contribution to journalArticle

27 Scopus citations

Abstract

The present studies test the hypothesis that contraction to EGF is dependent on mineralocorticoids and/or an elevation in systolic blood pressure (SBP). Endothelium-denuded thoracic aortas from sham normotensive, Nω-nitro-L-arginine (L-NNA) hypertensive, Wistar-Kyoto (WKY), and spontaneously hypertensive rats (SHR) were used in isolated tissue-bath experiments. Maximal contraction to epidermal growth factor [EGF; percentage of phenylephrine (PE; 10 umol/l)-induced contraction] was greater in strips from L-NNA (32 ± 5%) and SHR (53 ± 8%) rats compared with sham and WKY rats (17 ± 1 and 12 ± 4%, respectively). Wistar-Furth rats became only mildly hypertensive when given DOCA salt (134 ± 6 mmHg) compared with Wistar rats (176 ± 9 mmHg), but aortas from both strains had a similarly enhanced contraction to EGF (∼9 times the maximal contraction of sham aorta). Furthermore, in vitro incubation of aortas from Wistar and Wistar-Furth rats with aldosterone (10 nmol/l) increased EGF-receptor mRNA expression by >50%. These data indicate that arterial contraction to EGF may occur independent of hypertension and be stimulated by mineralocorticoids.

Original languageEnglish (US)
Pages (from-to)R878-R886
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume281
Issue number3 50-3
DOIs
StatePublished - 2001

Keywords

  • Hypertension
  • Vascular smooth muscle contraction
  • Wistar/Wistar-Furth rats

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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