Attenuated Ca2+ response to acetylcholine in endothelial cells from aorta of aldosterone-salt hypertensive rats

Yu Liu, Allan W. Jones, Michael Sturek

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

Ca2+ is essential for endothelial production of vasorelaxing factors. We determined whether the impaired endothelium-dependent relaxation in aldosterone-salt hypertensive rats (AHR) is associated with a decreased free Ca2+ ([Ca2+]i) response in endothelial cells. In isolated aorta, the EC50 for the acetylcholine-induced endothelium-dependent relaxations did not differ between AHR and the agematched control-salt rats (CSR). However, maximal relaxation was significantly reduced by 47% in AHR (P < .05). In contrast, the endothelium-independent relaxation to sodium nitroprusside was not impaired in aorta from AHR. The [Ca2+]i was measured with fura-2 microfluorometry in endothelial cells freshly dispersed from aorta. Although the basal [Ca2+]i was not different between CSR and AHR, the peak [Ca2+]i response to acetylcholine was significantly reduced in cells from AHR compared with CSR (P < .05). These results suggest that depressed endothelial [Ca2+]i responses to acetylcholine may be involved in the impaired endothelium-dependent relaxation in aorta from AHR.

Original languageEnglish (US)
Pages (from-to)404-408
Number of pages5
JournalAmerican Journal of Hypertension
Volume8
Issue number4
DOIs
StatePublished - Jan 1 1995
Externally publishedYes

Keywords

  • Fura-2
  • N-nitro L-arginine methyl ester
  • endothelium-dependent relaxation
  • indomethacin
  • sodium nitroprusside

ASJC Scopus subject areas

  • Internal Medicine

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