TY - JOUR
T1 - The impact of PCO2 and H+ on the release of acetylcholine from the cat carotid body
AU - Fitzgerald, Robert S.
AU - Shirahata, Machiko
AU - Chang, Irene
N1 - Funding Information:
This study was supported in part by research awards from the National Institutes of Health (NHLBI): HL-50712 and HL-72293.
PY - 2006/4/24
Y1 - 2006/4/24
N2 - The carotid body (CB) is a sensor of oxygen, carbon dioxide, hydrogen ion, and glucose in the arterial blood. Many studies of the CB's responses to low oxygen (hypoxia) have been reported. Recently attention has been increasingly focused on its responses to elevated CO2 (hypercapnia). An increase in ventilation or carotid body neural output (CBNO) can result from stimulating the CB with blood or perfusion fluids having an elevated CO2 or H+. The increase in ventilation seen with a hypoxic stimulus is accompanied with an increase in CBNO and an increased release of both acetylcholine (ACh) and ATP from the CB. The present in vitro study using both CBs harvested from six cats was undertaken to determine if hypercapnia also provoked an increased release of ACh from the incubated CBs. The anesthetizing, handling, and euthanizing of the animals were according to the guidelines of the Johns Hopkins Animal Care and Use Committee which are totally consonant with those of the NIH. CBs, once harvested and prepared for the experimental protocol, were subjected to the following steps each lasting 10 min: (1) control; (2) stress; (3) recovery. The stresses were respiratory acidosis (RAC; acidic hypercapnia), compensated respiratory acidosis (CRAC; isohydric hypercapnia), and metabolic acidosis (MtAC). The first and last forms of acidosis generated small but significant increases in the release of ACh from the CBs; the second generated a very small and insignificant increase in ACh release. Since it is generally accepted that ACh is a key excitatory neurotransmitter in the CB along with ATP, these data are consistent with other studies measuring the increase in ventilation in response to a small increase in CO2 and those studies recording CBNO in response to hypercapnia. In five of the six animals the responses to RAC and MtAC were compared to the responses to hypoxia. The latter were statistically indistinguishable from the former two.
AB - The carotid body (CB) is a sensor of oxygen, carbon dioxide, hydrogen ion, and glucose in the arterial blood. Many studies of the CB's responses to low oxygen (hypoxia) have been reported. Recently attention has been increasingly focused on its responses to elevated CO2 (hypercapnia). An increase in ventilation or carotid body neural output (CBNO) can result from stimulating the CB with blood or perfusion fluids having an elevated CO2 or H+. The increase in ventilation seen with a hypoxic stimulus is accompanied with an increase in CBNO and an increased release of both acetylcholine (ACh) and ATP from the CB. The present in vitro study using both CBs harvested from six cats was undertaken to determine if hypercapnia also provoked an increased release of ACh from the incubated CBs. The anesthetizing, handling, and euthanizing of the animals were according to the guidelines of the Johns Hopkins Animal Care and Use Committee which are totally consonant with those of the NIH. CBs, once harvested and prepared for the experimental protocol, were subjected to the following steps each lasting 10 min: (1) control; (2) stress; (3) recovery. The stresses were respiratory acidosis (RAC; acidic hypercapnia), compensated respiratory acidosis (CRAC; isohydric hypercapnia), and metabolic acidosis (MtAC). The first and last forms of acidosis generated small but significant increases in the release of ACh from the CBs; the second generated a very small and insignificant increase in ACh release. Since it is generally accepted that ACh is a key excitatory neurotransmitter in the CB along with ATP, these data are consistent with other studies measuring the increase in ventilation in response to a small increase in CO2 and those studies recording CBNO in response to hypercapnia. In five of the six animals the responses to RAC and MtAC were compared to the responses to hypoxia. The latter were statistically indistinguishable from the former two.
KW - Acetylcholine
KW - Acidic hypercapnia
KW - Carotid body
KW - Isohydric hypercapnia
KW - Metabolic acidosis
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U2 - 10.1016/j.neulet.2005.12.024
DO - 10.1016/j.neulet.2005.12.024
M3 - Article
C2 - 16406346
AN - SCOPUS:33644977873
SN - 0304-3940
VL - 397
SP - 205
EP - 209
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 3
ER -