Abstract — — The mouse is the most used animal for studying the genetic basis of cardiovascular diseases. However, the mechanisms of regulation of cardiovascular function in this animal are not yet well understood. The goal of this study was to evaluate the baroreflex, the Bezold-Jarisch cardiopulmonary reflex (BJR), and the chemoreflex in mice with hypertension induced by inhibition of NO using Nω -nitro- l -arginine-methyl ester (L-NAME). Basal mean arterial pressure (MAP) measured under anesthesia (urethane, 1 mg/g IP) was significantly higher in L-NAME (400 μg/g IP for 7 days)–treated (HT) mice (n=7) compared with vehicle-treated (NT; n=10) animals (126±9 versus 79±2 mm Hg) without differences in heart rate (HR). Baroreflex sensitivity, evaluated using phenylephrine (1 μg/g IV) was enhanced in HT mice compared with NT mice (−9.8±1.4 versus −4.9±0.5 bpm/mm Hg). The BJR, induced by phenylbiguanide (40 ng/g IV), was significantly attenuated in HT animals (MAP, −13±5%; HR, −39±6%) compared with NT animals (MAP, −38±5%; HR, −66±2%). The chemoreflex, induced by potassium cyanide (0.26 μg/g IV), was significantly attenuated in HT animals (MAP, +14±4%; HR, −8±2%) compared with NT animals (MAP, +29±4%; HR, −15±4%). As has been observed in rats, chronic inhibition of NO synthase in mice results in arterial hypertension. Enhancement of baroreflex sensitivity and attenuation of BJR and chemoreflex seem to be mainly caused by inhibition of NO synthesis because individual analyses did not show positive correlation between changes in these reflexes and MAP levels in the HT group.