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Central blockade of nitric oxide synthesis reduces moxonidine-induced hypotension
British Journal of Pharmacology (2004) 142,
Thiago Santos Moreira, Ana Carolina Thomaz Takakura, José V Menani, Monica Akemi Sato and Eduardo Colombari.
Department of Physiology, Universidade Federal de Sao Paulo – Escola Paulista de Medicina, 04023-060, Sao Paulo, SP, Brazil.
- Nitric oxide (NO) and 2-adrenoceptor and imidazoline agonists such as moxonidine may act centrally to inhibit sympathetic activity and decrease arterial pressure.
- 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.
- 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.
- Moxonidine (20 nmol), injected into the 4th V, reduced the mean arterial pressure (-423 mmHg), heart rate (-227 bpm) and renal (-6215%), mesenteric (-418%) and hindquarter (-508%) vascular resistances.
- Pretreatment with L-NAME (10 nmol into the 4th V) almost abolished central moxonidine-induced hypotension (-103 mmHg) and renal (-104%), mesenteric (-114%) and hindquarter (-136%) vascular resistance reduction, but did not affect the bradycardia (-188 bpm).
- 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.
Keywords: 2-Adrenoceptors, imidazoline receptors, hypertension, nitric oxide, blood flow, vascular resistance, blood pressure
