dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorMoreira, T. S.
dc.creatorTakakura, ACT
dc.creatorMenani, José Vanderlei
dc.creatorSato, M. A.
dc.creatorColombari, Eduardo
dc.date2014-05-20T13:45:41Z
dc.date2014-05-20T13:45:41Z
dc.date2004-06-01
dc.date.accessioned2017-04-05T20:53:11Z
dc.date.available2017-04-05T20:53:11Z
dc.identifierBritish Journal of Pharmacology. London: Nature Publishing Group, v. 142, n. 4, p. 765-771, 2004.
dc.identifier0007-1188
dc.identifierhttp://hdl.handle.net/11449/16084
dc.identifier10.1038/sj.bjp.0705853
dc.identifierWOS:000222532400016
dc.identifierWOS000222532400016.pdf
dc.identifierhttp://dx.doi.org/10.1038/sj.bjp.0705853
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/862979
dc.description1 Nitric oxide (NO) and alpha(2)-adrenoceptor and imidazoline agonists such as moxonidine may act centrally to inhibit sympathetic activity and decrease arterial pressure.2 In the present study, we investigated the effects of pretreatment with L-NAME ( NO synthesis inhibitor), injected into the 4th ventricle (4th V) or intravenously (i.v.), on the hypotension, bradycardia and vasodilatation induced by moxonidine injected into the 4th V in normotensive rats.3 Male Wistar rats with a stainless steel cannula implanted into the 4th V and anaesthetized with urethane were used. Blood flows were recorded by use of miniature pulsed Doppler flow probes implanted around the renal, superior mesenteric and low abdominal aorta.4 Moxonidine (20 nmol), injected into the 4th V, reduced the mean arterial pressure (-42+/-3 mmHg), heart rate (-22+/-7 bpm) and renal (-62+/-15%), mesenteric (-41+/-8%) and hindquarter (-50+/-8%) vascular resistances.5 Pretreatment with L-NAME (10 nmol into the 4th V) almost abolished central moxonidine-induced hypotension (-10+/-3 mmHg) and renal (-10+/-4%), mesenteric (-11+/-4%) and hindquarter (-13+/-6%) vascular resistance reduction, but did not affect the bradycardia (-18+/-8 bpm).6 the results indicate that central NO mechanisms are involved in the vasodilatation and hypotension, but not in the bradycardia, induced by central moxonidine in normotensive rats. British Journal of Pharmacology (2004).
dc.languageeng
dc.publisherNature Publishing Group
dc.relationBritish Journal of Pharmacology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectalpha(2)-adrenoceptors
dc.subjectimidazoline receptors
dc.subjecthypertension
dc.subjectnitric oxide
dc.subjectblood flow
dc.subjectvascular resistance
dc.subjectblood pressure
dc.titleCentral blockade of nitric oxide synthesis reduces moxonidine-induced hypotension
dc.typeOtro


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