Purinergic signalling mediates bidirectional crosstalk between chemoreceptor type I and glial-like type II cells of the rat carotid body.

摘要: Key points Carotid body chemoreceptors are organized in clusters containing receptor type I and contiguous glial-like II cells. While cells depolarize release ATP during chemostimulation, the role of which express purinergic P2Y2 receptors (P2Y2Rs) ATP-permeable pannexin-1 (Panx-1) channels, is unclear. Here, we show that isolated rat chemoreceptor clusters, cell depolarization induced by hypoxia, hypercapnia, or high K(+) caused delayed intracellular Ca(2+) elevations (Δ[Ca(2+)]i) nearby were inhibited P2Y2R blocker suramin, nucleoside hydrolase apyrase. Likewise, stimulation P2Y2Rs on a delayed, secondary Δ[Ca(2+)]i was blockers Panx-1 adenosine A2A 5'-ectonucleotidase. We propose reciprocal crosstalk between contributes to sensory processing carotid via signalling pathways. Abstract The mammalian (CB) excited blood-borne stimuli including hypoxia acid leading respiratory cardiovascular reflex responses. This chemosensory organ consists innervated cells, ensheathed processes adjacent major excitatory neurotransmitter released from (P2Y2Rs), activation leads opening ATP-permeable, channels. these properties support chemotransduction, direct evidence lacking. To address this, first exposed acute isohydric depolarizing stimulus K(+), monitored [Ca(2+)] using Fura-2. As expected, Interestingly, however, there often reversibly antagonist By contrast, with agonist uridine-5'-triphosphate (100 μm) led response carbenoxolone (5 μm). also strongly either (SCH 58261) 5'-ectonucleotidase (AOPCP), suggesting it due arising breakdown through Collectively, data suggest mechanisms mediate CB glial chemotransduction.