Premium
IMPACT OF CO2/H ON ACETYLCHOLINE (ACh) RELEASE FROM CAT CAROTID BODY (CB).
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-a
Subject(s) - hypercapnia , bicarbonate , acetylcholine , chemistry , carotid body , intracellular ph , hypoxia (environmental) , acidosis , endocrinology , medicine , intracellular , biochemistry , oxygen , biology , electrophysiology , organic chemistry
That the CB increases its neural output (CBNO) in response to both increased CO2 (acidic hypercapnia; AH) and increased H ion (metabolic acidosis; MA) is well known. Reports show that in response to isohydric hypercapnia (IH) CBNO rises abruptly but then tends to fall back towards a little above control. Since ACh is considered one of the essential excitatory neurotransmitters and its release increases in response to hypoxia, the present study explored the release of ACh in response to AH, MA, and IH. Bilateral CBs were removed from deeply anesthetized cats, prepared, and incubated at 37 deg. C in a Krebs Ringer bicarbonate solution (KRB), bubbled with 40% O2/5% CO2 for the initial control and the final recovery 10 min. periods. During the intervening 10 min challenges the KRB was bubbled with 40% O2/10% CO2 in normal bicarbonate (AH), with 40% O2/10%CO2 in elevated bicarbonate (IH), and with 40% O2/ 5%CO2 in decreased bicarbonate (MA). AH provoked a relatively small but significant increase in ACh release (23% greater than control). MA generated a significant increase in ACh release (28% greater than control). IH produced a very small and non‐significant increase in ACh release (5% greater than control). A concluding challenge by hypoxia (Krebs bubbled with 6% O2/5% CO2) stimulated a significant increase in ACh release (23% greater than control). These results are consistent with the behavior of CBNO, with the behavior of intracellular Ca2+ in the glomus cells and with their intracellular pH. The results suggest that ACh is a key excitatory neurotransmitter for CO2 and acidosis. Supported by NIH awards HL 50712 and HL 72293.