Abstract
The carotid body is a multi-modal sensor and it has been debated if it senses low glucose. We have hypothesized that the carotid body is modified by some metabolic factors other than glucose and contributes to whole body glucose metabolism. This study examined the roles of insulin, leptin and transient receptor potential (TRP) channels on carotid sinus nerve (CSN) chemoreceptor discharge. In agreement with other studies, CSN activity was not modified by low glucose. Insulin did not affect the CSN hypoxic response. Leptin significantly augmented the CSN response to hypoxia and nonspecific Trp channel blockers (SKF96365, 2-APB) reversed the effect of leptin. Gene expression analysis showed high expression of Trpm3, 6, and 7 channels in the carotid body and petrosal ganglion. The results suggest that the adult mouse carotid body does not sense glucose levels directly. The carotid body may contribute to neural control of glucose metabolism via leptin receptor-mediated TRP channel activation.