The functional integrity of extrathoracic airways critically depends on the proper orchestration of the activities of a set of patency-maintaining muscles. Recruitment and control of these muscles is regulated by a laryngeal and trigeminal affects that originate from pressure sensing endings. These sensors are particularly numerous among laryngeal receptors and, indeed, they constitute the main element in the respiration-modulated activity of the superior laryngeal nerve. Considering that the most compliant region of the upper airway, and thus more vulnerable to inspiratory collapse, lies cranially to the larynx, the laryngeal pressure-sensing endings seem to be ideally located for detecting collapsing forces and initiating reflex mechanisms for the preservation of patency. This process operates by activating upper airway dilating muscles and by decreasing inspiratory drive: both actions limit t he effect of the collapsing forces. Cold reception is differently represented in various mammalian species within nasal and laryngeal segments. Cooling of the upper airway has an inhibitory influence on breathing, especially in newborns, and a depressive effect on upper airway dilating muscles. The latter response is presumably mediated through the inhibitory effect of cooling on laryngeal pressure endings. These responses could be harmful during occlusive episodes. Powerful defensive responses with distinct characteristics can be elicited through the simulation of laryngeal and nasal irritant type receptors. Sneezing is elicited through the stimulation of trigeminal afferents, cough through the stimulation of laryngeal vagal endings. Changes in osmolality and ionic composition of the mucosal surface liquid can lead to conspicuous alterations in receptor activity and related reflexes.