An adequate supply of oxygen (02) is essential to the survival of all higher
organisms. The mammalian carotid body, located at the common carotid artery senses
blood levels of 0 2, carbon dioxide (C02) and acidity. Glomus cells, or type I cells in the
carotid body are the main 0 2-sensors which regulate blood p02 via reflex control of
ventilation. The carotid body secretes multiple neurotransmitters including dopamine
(DA), which is potentiated during low p02 levels and is thought to modulate sensory
signaling by apposing afferent nerve fibers. Catecholamine (CA) release is also critical
for the animal's ability to survive hypoxic stress associated with the birthing process and
the transition to extrauterine life. However, the source for this CA release (primarily
epinephrine; EPI) is from adrenal chromaffin cells. The primary 02-sensor in both
adrenal chromaffin cells and carotid body type I cells is unknown. One potential
candidate is the cytochrome b55s/NADPH oxidase complex that generates the respiratory
burst in phagocytes. To test this hypothesis, cultured adrenal medulla chromaffin cells
and intact carotid bodies from wild type (WT) and oxidase deficient (OD) mice
(knockout gp91 phox, the glycoprotein subunits in the NADPH oxidase complex) were
investigated. High performance liquid chromatography and immunocytochemistry were
used to quantify amine release in these two chemoreceptors following exposure to
hypoxia. Both WT and OD chromaffin cells and carotid bodies responded to the hypoxic
challenge with increased monoamine secretion. Norepinephrine and epinephrine were the
principal amines released from chromaffin cells, compared to dopamine and serotonin
from carotid bodies. These findings suggest that NADPH oxidase is not the primary 02-
sensor in either chemosensory system. Quantification of monoamine secretion in intact
carotid body from mouse and rat was also compared under basal conditions and after
exposure to hypoxia and acid/hypercapnia (pH 7.10). Significantly larger amounts of
basal serotonin was secreted from mouse carotid body as compared to the rat.
Interestingly, serotonin release was potentiated by hypoxia in mouse carotid body, but
this was not observed in the rat. Additionally, ratio of basal level serotonin-to-dopamine
secretion was significantly higher in mouse than rat CB. Surprisingly, acid/hypercapnic
(pH 7.1 0) had no detectable effect on amine secretion from either mouse or rat carotid
body. / Thesis / Master of Science (MSc)
| Identifer | oai:union.ndltd.org:mcmaster.ca/oai:macsphere.mcmaster.ca:11375/22612 |
| Date | January 2000 |
| Creators | Farragher, Suzanne |
| Contributors | Nurse, Colin A., Biology |
| Source Sets | McMaster University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis |
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