Cardiovascular dysfunction associated with obesity was assessed by comparing rats that had been maintained on a regular or high fat diet since weaning. Rats on the high fat diet not only gained weight faster than age-matched controls but also had higher systolic and mean pressures. Development of mild hypertension in obese rats was first detected by indirect tail-cuff measurement and confirmed later by recording intra-arterial pressures directly from indwelling femoral catheters. To assess baroreceptor reflex sensitivity, reflex heart rate responses were elicited by lowering blood pressure with sodium nitroprusside or elevating it with phenylephrine. Initial tests showed that, although reflex tachycardia during depressor responses to sodium nitroprusside did not differ between groups, reflex bradycardia during pressor responses to phenylephrine was weaker in obese than in control rats. Underlying autonomic mechanisms were then examined by repetition of baroreceptor reflex tests after cholinergic blockade with methylatropine or β-adrenergic blockade with propranolol. Reflex tachycardia was equally inhibited in both groups by either antagonist. By contrast, reflex bradycardia was reduced more in obese than in control rats by β-adrenergic blockade but was equally reduced by cholinergic blockade. Because residual responses after β-adrenergic blockade would represent remaining parasympathetic mediation, these results indicate that reflex bradycardia was selectively impaired because of deficient parasympathetic mediation. Considered collectively, our results suggest that impaired parasympathetic mediation of reflex bradycardia could either result from or contribute to the blood pressure elevation in obese rats.