The ECS is expressed both centrally in the preBotzinger complex and nucleus tractus solitarius and extensively in peripheral tissues of the respiratory system. Activation of CB1 receptor in the preBotzinger complex and nucleus tractus solitarius in experimental models did lead to respiratory depression. This was mitigated by CB2 activation in microglial cells of the same area. AEA inhibition of the K+ channel receptor TWIK-related acid-sensitive potassium channel (TASK-1) receptor appears to have beneficial effects in OSA, increasing respiratory drive. AEA also activated TRPV1 receptors in the carotid body in response to exercise to increase respiratory drive. Activation of CB1 in bronchioles in animal models can lead to bronchoconstriction if airways are already relaxed or bronchodilation if they were previously constricted. Human studies have demonstrated similar mixed effects. The ECS again plays an important role in managing inflammation in the lungs, and studies in animals suggest an overall benefit in asthmatic models with endocannabinoid activation of CB1, CB2, and PPAR but not TRPV1, which has detrimental effects.