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Received April 4, 2002
Accepted after revision June 18, 2002
1 Department of Physiology, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, UK
2 Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, 14049-900, Ribeirao Preto, Sao Paulo, Brazil
3 Department of Physiology, Royal Free and University College Medical School, University College London, London NW3 2PF, UK
4 Department of Physiology, School of Medical Sciences, University of Bristol, Bristol BS8 2TD, UK
* To whom correspondence should be addressed. E-mail: julian.f.r.paton{at}bris.ac.uk.
We have assessed the functional role of type 2 purinergic (P2) receptors within the caudal aspect of the commissural nucleus tractus solitarii (NTS) in mediating the peripheral chemoreceptor reflex cardiorespiratory response in the arterially perfused in situ working heart-brainstem preparation of rats. Microinjection in NTS of either suramin (100 pmol) or pyrinoxalphosphate-6-azophenyl-2â,4â-disulphonic acid tetrasodium salt (PPADS; 10 pmol) depressed the reflex bradycardia (by ~50 %), but not the tachypnoea, following peripheral chemoreceptor stimulation. In contrast, the reflex bradycardia produced by stimulation of pharyngo-oesophageal receptors was unaffected. Furthermore, microinjections in NTS of the P2X receptor agonist 
,ß-methyleneadenosine 5â-triphosphate (10 pmol) evoked a bradycardia which was antagonized by suramin (100 pmol). This P2X agonist reversibly potentiated the peripheral chemoreceptor-evoked bradycardia. The effect of suramin was selective to purinergic receptors because the bradycardia evoked by microinjection of ,ß-methyleneadenosine 5â-triphosphate was blocked while the bradycardic responses to microinjections of NMDA or non-NMDA receptor agonists were not affected. From whole-cell recordings, some NTS neurones received convergent excitatory synaptic inputs from both peripheral chemoreceptors and receptors at the pharyngo-oesophageal junction. The excitatory postsynaptic response evoked by chemoreceptor stimulation was depressed by suramin, but convergent excitatory inputs from pharyngo-oesophageal receptors were unperturbed. Our findings support the hypothesis that caudal commissural NTS P2 purinergic receptors play a role in the neurotransmission of the parasympathetic (bradycardic) component of the chemoreceptor reflex. This effect is highly selective in that the chemoreceptor afferent-evoked tachypnoea, as well as other visceral receptor-mediated reflex bradycardia, remain unaffected.
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