1. 17β-Estradiol Decreases Nitric Oxide Synthase II Synthesis in Vascular Smooth Muscle Cells*
- Author
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Sabrina Santagati, Elisabetta Vegeto, Lina Puglisi, Valeria Zancan, Adriana Maggi, and Chiara Bolego
- Subjects
Male ,medicine.medical_specialty ,Vascular smooth muscle ,Endothelium ,medicine.medical_treatment ,Nitric Oxide Synthase Type II ,Biology ,Muscle, Smooth, Vascular ,Rats, Sprague-Dawley ,Endocrinology ,Internal medicine ,medicine.artery ,medicine ,Animals ,RNA, Messenger ,Fulvestrant ,Aorta ,Cells, Cultured ,Nitrites ,Progesterone ,Estradiol ,Estrogen Antagonists ,Antagonist ,17beta estradiol ,Rats ,Nitric oxide synthase ,Tamoxifen ,medicine.anatomical_structure ,Cytokine ,Receptors, Estrogen ,cardiovascular system ,biology.protein ,Nitric Oxide Synthase ,Hormone - Abstract
Several studies have provided evidence for a direct effect of 17beta-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 17beta-estradiol on inducible NOS (NOS II) in primary culture of smooth muscle cells (SMC) from rat aorta. We here prove that 17beta-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 17beta-estradiol effect. On the other hand, progesterone is deprived of any effect on NOS II content or activity, proving the specificity of 17beta-estradiol effect. In addition, we show that 17beta-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.
- Published
- 1999
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