The Anti-Tachycardic Mechanism of a Direct-Acting Vasodilator, Budralazine, in Rats

Abstract

The present study was undertaken to elucidate the anti-tachycardic effect of a direct-acting vasodilator, budraiazine, using an electrophysiological technique. Normotensive male Wistar rats were used. Rats were anesthetized intraperitoneally with urethane and α-chloralose. Intravenous administration of budralazine (0.5–5.0mg/kg) produced a dose-dependent reduction of mean arterial pressure in anesthetized rats. At doses of 0.5 and 1.0 mg/kg, budralazine induced bradycardia accompanied with a decrease in cardiac sympathetic nerve activity (ICNA). Preganglionic adrenal sympathetic nerve activity (ASNA) was also reduced by budralazine (1.0mg/kg). A 0.5mg/kg of budralazine neither influenced carotid sinus nerve activity nor augmented aortic depressor nerve activity (ADNA). On the contrary, at dose of 5.0 mg/kg, budralazine produced a tachycardia accompanied with increases in both ICNA and ASNA. The ADNA was decreased by budralazine (5.0mg/kg) significantly. These findings suggest that the central sympatnoinhibitory action of budralazine may be responsible for the anti-tachycardic effect of budralazine and baroreceptor-mediated tachycardia occurred after high dose of budralazine.

Key Words:

• vasodilator
• blood pressure
• heart rate
• sympathetic nerve activity
• baroreflex
• hydralazine
• budralazine