scholarly journals Muscarinic and nicotinic receptors raise intracellular Ca2+ levels in rat carotid body type I cells.

1997 ◽  
Vol 498 (2) ◽  
pp. 327-338 ◽  
Author(s):  
L L Dasso ◽  
K J Buckler ◽  
R D Vaughan-Jones
Keyword(s):  
Carotid Body ◽  
Nicotinic Receptors ◽  
Type I ◽  
Body Type ◽  
Type I Cells ◽  
Muscarinic And Nicotinic Receptors ◽  
I Cells

A standing Na+ conductance in rat carotid body type I cells

Neuroreport ◽  
2001 ◽  
Vol 12 (7) ◽  
pp. 1421-1425 ◽  
Author(s):  
Elisabeth Carpenter ◽  
Chris Peers
Keyword(s):  
Carotid Body ◽  
Type I ◽  
Body Type ◽  
Type I Cells ◽  
I Cells

Enhanced adenosine A2breceptor signaling facilitates stimulus-induced catecholamine secretion in chronically hypoxic carotid body type I cells

2013 ◽  
Vol 305 (7) ◽  
pp. C739-C750 ◽  
Author(s):  
Simon Livermore ◽  
Colin A. Nurse
Keyword(s):  
Carotid Body ◽  
Catecholamine Secretion ◽  
Receptor Blocker ◽  
Type I ◽  
Dependent Manner ◽  
Body Type ◽  
Type I Cells ◽  
High K ◽  
Sch 58261 ◽  
I Cells

Chronic hypoxia (CHox) augments chemoafferent activity in sensory fibers innervating carotid body (CB) chemoreceptor type I cells; however, the underlying mechanisms are poorly understood. We tested the hypothesis that enhanced paracrine signaling via adenosine (Ado) A2breceptors is involved. Dissociated rat CB cultures were exposed for 24 h to normoxia (Nox, 21% O2) or CHox (2% O2) or treated with the hypoxia mimetic deferoxamine mesylate (DFX), and catecholamine secretion from type I cells was monitored by amperometry. Catecholamine secretion was more robust in CHox and DFX type I cells than Nox controls after acute exposure to acid hypercapnia (10% CO2, pH 7.1) and high K+(75 mM). Exogenous Ado increased catecholamine secretion in a dose-dependent manner, and the EC50was shifted to the right from ∼21 μM Ado in Nox cells to ∼78 μM in CHox cells. Ado-evoked secretion in Nox and CHox cells was markedly inhibited by MRS-1754, an A2breceptor blocker, but was unaffected by SCH-58261, an A2areceptor blocker. Similarly, MRS-1754, but not SCH-58261, partially inhibited high-K+-evoked catecholamine secretion, suggesting a contribution from paracrine activation of A2breceptors by endogenous Ado. CB chemostimuli, acid hypercapnia, and hypoxia elicited a MRS-1754-sensitive rise in intracellular Ca2+that was more robust in CHox and DFX than Nox cells. Taken together, these data suggest that paracrine Ado A2breceptor signaling contributes to stimulus-evoked catecholamine secretion in Nox and CHox CB chemoreceptors; however, the effects of Ado are more robust after CHox.

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