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We have previously shown that activation of P2X purinoceptors in the subpostremal nucleus tractus solitarius (NTS) produces a rapid bradycardia and hypotension. This bradycardia could occur via sympathetic withdrawal, parasympathetic activation, or a combination of both mechanisms. Thus we investigated the relative roles of parasympathetic activation and sympathetic withdrawal in mediating this bradycardia in chloralose-urethane anesthetized male Sprague-Dawley rats. Microinjections of the selective P2X purinoceptor agonist [alpha], [beta]-methylene ATP (25 pmol/50 nl and 100 pmol/50 nl) were made into the subpostremal NTS in control animals, after atenolol (2 mg/kg iv), a [beta]-selective antagonist, and after atropine methyl bromide (2 mg/kg iv), a muscarinic receptor antagonist. The bradycardia observed with activation of P2X receptors at the low dose of the agonist is mediated almost entirely by sympathetic withdrawal. After [[beta].sub.1]-adrenergic blockade, the bradycardia was reduced to just -5.1 [+ or -] 0.5 versus -28.8 [+ or -] 5.1 beats/min in intact animals. Muscarinic blockade did not produce any significant change in the bradycardic response at the low dose. At the high dose, both [[beta].sub.1]-adrenergic blockade and muscarinic blockade attenuated the bradycardia similarly, -37.4 [+ or -] 6.4 and -40.6 [+ or -] 3.7 beats/min, respectively, compared with -88.0 [+ or -] 11 beats/min in control animals. Double blockade of both [[beta].sub.1]-adrenergic and muscarinic receptors virtually abolished the response (-2.5 [+.sub. -] 0.8 beats/min). We conclude that the relative contributions of parasympathetic activation and sympathetic withdrawal are dependent on the extent of P2X receptor activation. heart rate; nucleus tractus solitarius; [alpha],[beta]-methylene adenosine 5'triphosphate