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1 Departamento de Farmacologia y Terapeutica, Universidad Autonoma de Madrid, Madrid, Spain
2 Departamento de Ciencias de la Salud, Universidad Rey Juan Carlos, Alcorcon, Madrid, Spain
3 Departament de Farmacologia, Terapeutica i Toxicologia, Universitat Autonoma de Barcelona, Barcelona, Spain
* To whom correspondence should be addressed. E-mail: mercedes.salaices{at}uam.es.
This study was performed to investigate the role of reactive oxygen species and inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX-2) metabolites in the LPS effect on bradykinin-induced relaxation in middle cerebral arteries from normotensive (WKY) and spontaneously hypertensive rats (SHR). LPS (1-5 h, 10 µg/ml) reduced bradykinin relaxation; this effect appeared earlier and was greater in arteries from SHR than WKY. LPS also reduced the relaxation to the NO donor, DEA-NO; however, LPS modified neither the bradykinin relaxation after inhibiting NO synthesis with L-NMMA (0.1 mM) nor eNOS expression. In arteries from WKY, the respective iNOS and COX-2 inhibitors, aminoguanidine (0.1 mM) and NS 398 (10 µM), and the superoxide anion scavenger, SOD (100 U/ml), reduced the LPS effect on bradykinin relaxation; however, the TXA2/PGH2 receptor antagonist, SQ 29,548 (1 µM), and the hydrogen peroxide scavenger, catalase (1000 U/ml), did not modify the LPS effect. In arteries from SHR, all these drugs reduced the LPS effect. LPS (5 h) increased superoxide anion levels in arteries from both strains and TXA2 levels only in SHR. COX-2 expression rose to a similar level in arteries from both strains after 1 and 5 h LPS incubation, while expression of Cu/Zn- and Mn-SOD only increased after 5 h. In conclusion, in segments from WKY, LPS reduced bradykinin-induced relaxation through increased production of NO from iNOS and of superoxide anion. The greater LPS effect observed in arteries from SHR seems to be related to higher participation of reactive oxygen species and contractile prostanoids, probably TXA2.
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