17 beta-estradiol-stimulated nitric oxide production by neutrophils: Effect on platelet activation

Citation
Mg. Duran et al., 17 beta-estradiol-stimulated nitric oxide production by neutrophils: Effect on platelet activation, OBSTET GYN, 95(2), 2000, pp. 284-290
Citations number
39
Categorie Soggetti
Reproductive Medicine","da verificare
Journal title
OBSTETRICS AND GYNECOLOGY
ISSN journal
00297844 → ACNP
Volume
95
Issue
2
Year of publication
2000
Pages
284 - 290
Database
ISI
SICI code
0029-7844(200002)95:2<284:1BNOPB>2.0.ZU;2-S
Abstract
Objective: To evaluate the effect of 17 beta-estradiol (E2) on the ability of human neutrophils to produce nitric oxide (NO) and its effects on platel et activation. Methods: The expression of neuronal nitric oxide synthase (nNOS) protein an d the formation of NO by 17 beta-E2-incubated neutrophils from men were stu died in vitro (ten male volunteers, no medical-surgical antecedents, aged 2 5-45 years). Platelet aggregometry and changes in cyclic guanosine monophos pate (cGMP) levels were used to bioassay the functionality of NO released f rom neutrophils. Results: Incubation of neutrophils derived from men with physiologic concen trations of 17 beta-E2 (10(-10) to 10(-8) mol/L) enhanced the expression of nNOS protein. 17 beta-E2-incubated neutrophils also showed a significant i ncrease in their ability to generate NO measured by the conversion of [H-3] -L-arginine to [H-3]-L-citrulline. Furthermore, 17 beta-E2-incubated neutro phils showed a greater ability to prevent adenosine diphosphate (ADP)-induc ed platelet activation. Moreover, increased levels of cGMP were found in th e coincubation of platelets with 17 beta-E2-treated neutrophils. Conclusion: These results suggest that 17 beta-E2 increases the ability of human neutrophils to produce NO and therefore may contribute to cardiovascu lar disease protection. (Obstet Gynecol 2000;95:284-90. (C) 2000 by The Ame rican College of Obstetricians and Gynecologists.).