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Sensory Afferent Selective Role of P2 Receptors in the Nucleus Tractus Solitarii for Mediating the Cardiac Component of the Peripheral Chemoreceptor Reflex in Rats
Author(s) -
Paton Julian F. R.,
Paula Patrícia M.,
Spyer K. Michael,
Machado Benedito H.,
Boscan Pedro
Publication year - 2002
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2002.021923
Subject(s) - reflex bradycardia , chemoreceptor , ppads , purinergic receptor , solitary nucleus , medicine , endocrinology , reflex , stimulation , biology , p2 receptor , excitatory postsynaptic potential , neuroscience , receptor , bradycardia , inhibitory postsynaptic potential , heart rate , adenosine , blood pressure
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‐2′,4′‐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 α,β‐methyleneadenosine 5′‐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 α,β‐methyleneadenosine 5′‐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.