Capsaicin produces complex Triphasic cardio-respiratory responses characterized by immediate hypotension associated with apnea, intermediate recovery with bradypnea and delayed hypotension with tachypnea. However, the mechanisms underlying this complex cardio-respiratory responses are not clear. Therefore, this study was undertaken to delineate the mechanisms involved in capsaicin-induced respiratory response in connection to pressure responses. Tracheal, jugular venous and femoral artery cannulations were performed in urethane anaesthetized adult rats. Blood pressure, and respiratory excursions were recorded. Jugular venous injection of capsaicin (10µg/kg) produced Triphasic pressure response exhibiting immediate hypotension, intermediate recovery and delayed hypotension. Time-matched respiratory changes showed apnea, bradypnea and tachypnea, respectively. After vagotomy, immediate hypotension was abolished; the intermediate recovery in presser response was augmented as hypertensive response; and the delayed hypotension persisted. In these animals, immediate apnea was attenuated, intermediate apnea/bradypnea persisted and delayed tachypnea was abolished after vagotomy. Antagonists of 1-Adrenoceptor (proposing, 0.5mg/kg) or AT1 receptor (losartan, 10mg/kg) did not block the capsaicin-induced intermediate hypertensive response as well as apnea/bradypnea in vagotomized animals. The present observations indicate that capsaicin-induced intermediate hypertensive response in association with apnea/bradypnea in vagotomized animals is not mediated through adrenergic and angiotensinergic mechanisms. The direct modulation of central respiratory area may be a possibility.