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Sympathetic and parasympathetic component of bradycardia triggered by stimulation of NTS P2X receptors

Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan

Submitted 19 August 2005 ; accepted in final form 23 September 2005

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 ,-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 ₁-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 ₁-adrenergic blockade, the bradycardia was reduced to just –5.1 ± 0.5 versus –28.8 ± 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 ₁-adrenergic blockade and muscarinic blockade attenuated the bradycardia similarly, –37.4 ± 6.4 and –40.6 ± 3.7 beats/min, respectively, compared with –88.0 ± 11 beats/min in control animals. Double blockade of both ₁-adrenergic and muscarinic receptors virtually abolished the response (–2.5 ± 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; ,-methylene adenosine 5'triphosphate

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