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The Effect of Obese Levels of Leptin on Peripheral Chemoreception

Obesity rates are increasing rapidly worldwide. Breathing and cardiovascular systems’ function are directly impacted by obesity and contribute to obesity related pathology. Leptin receptors are present in the oxygen sensing type I cells of the carotid body and in carotid sinus nerve afferent fibers. The adipokine leptin is a respiratory stimulant with known central effects. We have previously reported that acute administration of obese levels of leptin causes a measurable and long lasting change in Ca2+ signal in isolated carotid body type I cells as well as augmenting BKCa channel activity. Here we report that 100nM wortmannin, a PI3K inhibitor, blocks leptin induced Ca2+ signaling in these cells. Furthermore we show that in an ex‐vivo arterially perfused carotid body preparation that leptin causes a dose dependent increase in baseline firing rates under normoxia and an increase in the size of the sensory response to hypoxic challenge that does not wash out. These data show that leptin alters carotid body function acutely and suggest that studying carotid body function in chronic models of obesity is warranted.