Several studies have provided evidence fur a direct effect of 17 beta-estradiol on vessel wall via interaction with the constitutively expressed nitric oxide synthase (NOS) by endothelium. The aim of the present study was to investigate the effect of 17 beta-estradiol on inducible NOS (NOS II) in primary culture of smooth muscle cells (SMC) fram rat aorta. We here prove that 17 beta-estradiol decreases the content and activity of NOS II in SMC. This effect appears to be the consequence of ER activation, because: 1) ER alpha: and ER beta are expressed in rat aorta SMC grown in culture; 2) low concentrations of hormone modulate NOS II activity; 3) the specific ER alpha antagonist ICI182,780 completely blocks 17 beta-estradiol effect, On the other hand, progesterone is deprived of any effect on NOS II content or activity, proving the specificity of 17 beta-estradiol effect. In addition, we show that 17 beta-estradiol can counteract the increase in NOS II activity following cytokine treatment. The observation could indicate a novel mechanism for the protective effects exerted by these hormones in cardiovascular diseases and atherosclerosis in particular.

17 beta-estradiol decreases nitric oxide synthase II synthesis in vascular smooth muscle cells / V. Zancan, S. Santagati, C. Bolego, E. Vegeto, A. Maggi, L. Puglisi. - In: ENDOCRINOLOGY. - ISSN 0013-7227. - 140:5(1999), pp. 2004-2009.

17 beta-estradiol decreases nitric oxide synthase II synthesis in vascular smooth muscle cells

E. Vegeto;A. Maggi;
1999

Abstract

Several studies have provided evidence fur a direct effect of 17 beta-estradiol on vessel wall via interaction with the constitutively expressed nitric oxide synthase (NOS) by endothelium. The aim of the present study was to investigate the effect of 17 beta-estradiol on inducible NOS (NOS II) in primary culture of smooth muscle cells (SMC) fram rat aorta. We here prove that 17 beta-estradiol decreases the content and activity of NOS II in SMC. This effect appears to be the consequence of ER activation, because: 1) ER alpha: and ER beta are expressed in rat aorta SMC grown in culture; 2) low concentrations of hormone modulate NOS II activity; 3) the specific ER alpha antagonist ICI182,780 completely blocks 17 beta-estradiol effect, On the other hand, progesterone is deprived of any effect on NOS II content or activity, proving the specificity of 17 beta-estradiol effect. In addition, we show that 17 beta-estradiol can counteract the increase in NOS II activity following cytokine treatment. The observation could indicate a novel mechanism for the protective effects exerted by these hormones in cardiovascular diseases and atherosclerosis in particular.
Settore BIO/14 - Farmacologia
1999
Article (author)
File in questo prodotto:
File Dimensione Formato  
Zancan 1999.pdf

accesso aperto

Tipologia: Publisher's version/PDF
Dimensione 471.19 kB
Formato Adobe PDF
471.19 kB Adobe PDF Visualizza/Apri
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/189415
Citazioni
  • ???jsp.display-item.citation.pmc??? 13
  • Scopus 78
  • ???jsp.display-item.citation.isi??? 70
social impact