Angiotensin II (ANG II) stimulates ventilation (V), when ventilatory baroreceptor reflexes are taken into account, and arginine vasopressin (AVP) causes baroreflex inhibition of V in conscious and anesthetized dogs. To study mechanisms of hormonal modulation of V, a conscious rat model was investigated. V and metabolism were measured during steady-state intravenous infusions of ANG II and AVP in Sprague-Dawley rats (mean arterial pressure (MAP) increased 20 mmHg (1 mmHg = 133.3 Pa)). These data were compared with observations during equal pressor infusions of phenylephrine (PE), an agent classically used to study baroreceptor reflexes. V, respiratory frequency (f), and tidal volume (Vt) were maintained during the increased MAP associated with ANG II infusions, a response identical with that reported in conscious dogs. However, unlike dogs, AVP infusion did not depress V and metabolism in rats. PE in conscious rats caused an unexpected increase in Vt and V in association with increased metabolism. None of the pressor agents affected breath timing when the latter was binned by breath f. Since there was no obvious baroreflex inhibition of V with AVP and PE, potential stimulatory effects of ANG II on respiration could not be discerned. As well, the ventilatory baroreceptor pressure threshold may be higher or adaptation of the reflex may be faster in conscious rats than in dogs.