ABSTRACT
The carotid body is the primary sensor of hypoxemia across many species. When stimulated by a decrease in PaO2, or hypoxic perfusates, it promotes many cardiopulmonary responses. Ventilation, static lung volumes, airway resistance, and airway secretions increase. The hypoxic pulmonary vasoconstrictor response and the systemic vascular vasodilator responses are attenuated; bronchial vascular resistance decreases (for review see Ref. 1). A current question is: How does the carotid body transduce a low PaO2, stimulus into increased neural output traveling to the nucleus tracrus solitarii? Here the increased neural traffic is processed and distributed to various other nuclei responsible for the increased breathing and the autonomically regulated changes in the cardiopulmonary system.
