Influence of hypoxia/low glucose on carotid body release of acetylcholine

Abstract

The carotid body (CB), a polymodal sensor of arterial blood, increases its neural output to the brain when stimulated by low O2 tension, pH, glucose, or high CO2 tension. Reflex cardiopulmonary responses ensue. Current reports identify acetylcholine (ACh) and ATP as two excitatory transmitters in the cat and rat CBs. This study explored the impact of hypoxia (HH), low glucose, and both together on the release of ACh and ATP from two incubated cat CBs. The CBs were prepared with standard procedures consonant with the regulations of the Institutional Animal Care and Use Committee. ACh was measured with HPLC-ECD methods. ATP was measured with luminometer for bioluminescence. Normalized to their controls, significantly increased ACh samples were recovered from the incubation medium in response to HH, low glucose, and HH+low glucose. Normalized to their controls, significantly increased ATP samples were recovered from the incubation medium in response to HH and HH+low glucose. Low glucose generated an increase in ATP which was not significant at the 0.05 level. Further, normalizing the initial challenge stage to the final control stage for both ACh and ATp generated significant increases in response to HH, low glucose (ACh only), and HH+low glucose. The data suggest the release of both transmitters is relatively constant under the conditions of the experiments. Further, they suggest the increased neural output in response to low glucose is primarily, if not exclusively, due to ACh. Supported by NIH awards from NHLBI: HL 05-0712-13, HL72293.