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INTERACTION OF ACETYLCHOLINE (ACh) AND ADENOSINE (ADO) ON GLOMUS CELL INTRACELLULAR CALCIUM (Cai).
Author(s) -
Fitzgerald Robert Schaefer,
Shirahata Machiko,
Chang Irene
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a784-b
Subject(s) - muscarinic acetylcholine receptor , agonist , acetylcholine , methyllycaconitine , medicine , chemistry , endocrinology , muscarinic acetylcholine receptor m3 , adenosine , receptor , ritanserin , receptor antagonist , pharmacology , antagonist , nicotinic agonist , biology , nicotinic acetylcholine receptor
Carotid body (CB) glomus cells (GCs) contain several neurotransmitters. In the CB released ATP metabolizes into ADO. GCs exhibit both ADO and ACh autoreceptors, and stimulation of both nicotinic and muscarinic autoreceptors raises [Ca]i in GCs. The present study examined how ADO might modify the impact of ACh on [Ca]i in cat GCs. Bilateral CBs were harvested from deeply anesthetized 3–4 month old cats and cultured. GC‐containing slides were incubated with Fura 2 dye. Standard micrfluorometry was used to determine the changes in [Ca]i in responses to ACh plus ADO and ACh plus ADO receptor agents. The GCs were perfused with stimulant for 1 min followed by 14 min of rest with KRB. Response was recorded for 5 min. Three successive perfusions of 100 microM ACh produced a progressive decline in the rise of [Ca]i. Inclusion of 100 microM ADO with the ACh prevented this decline. Inclusion of ADO along with ACh and an A1 receptor antagonist, DPCPX, not only prevented the decline, but promoted an increase in the ACh effect on [Ca]i. Inclusion of the A2a ADO receptor agonist, CGS21680, with ACh also prevented the decline in [Ca]i. These data suggest that ADO and the A2a ADO receptor agonist, along with the A1 ADO receptor antagonist may attenuate the desensitization of the ACh nicotinic receptors. Or ADO may work through the muscarinic receptors as well. Supported by NIH awards: HL 50712, HL 72293.