17β-Estradiol increases nitric oxide-dependent dilation in rat pulmonary arteries and thoracic aorta

Rayna J. Gonzales, Benjimen R. Walker, Nancy L. Kanagy

Research output: Contribution to journalArticlepeer-review

49 Scopus citations

Abstract

Past studies have demonstrated that 17β-estradiol (E2β) increases endothelial nitric oxide (NO) synthase (eNOS) activity in uterine, heart, and skeletal muscle and in cultured human endothelial cells. However, little is known about E2β regulation of NO synthesis in the pulmonary vasculature. The present study evaluated E2β regulation of eNOS function in pulmonary arteries and thoracic aortas. We hypothesized that E2β upregulates vascular NO release by increasing eNOS expression. To test this, NO-dependent vasodilation was assessed in isolated perfused lungs and aortic rings from ovariectomized Sprague-Dawley rats treated for 1 wk with 20 μg/24 h of E2β or vehicle. Expression of eNOS was evaluated by Western blot and immunohistochemistry. Also, a RNase protection assay determined eNOS mRNA levels in lung and aortic homogenates from control and treated rats. Vasodilation to ionomycin in lungs from the E2β-treated group was enhanced compared with that in control animals. Endothelium-intact aortic rings from E2β-treated animals also demonstrated augmented endothelium-dependent dilation. Both responses were blocked with NOS inhibition. Immunostaining for eNOS was greater in pulmonary arteries and aortas from E2β-treated compared with control rats. However, mRNA levels did not differ between groups. Thus we conclude that in vivo E2β treatment augments endothelium-dependent dilation in aorta and lung, increasing expression of eNOS independently of sustained augmented gene transcription.

Original languageEnglish (US)
Pages (from-to)L555-L564
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume280
Issue number3 24-3
DOIs
StatePublished - Mar 2001

Keywords

  • Endothelial nitric oxide synthase
  • Endothelium-dependent vasodilation
  • Isolated rat lungs

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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