Peripheral chemoreceptors (carotid and aortic bodies) and central chemoreceptors (medullary neurons) primarily function to regulate respiratory activity. This is an important mechanism for maintaining arterial blood PO2, PCO2, and pH within appropriate physiological ranges. For example, a fall in arterial PO2 (hypoxemia) or an increase in arterial PCO2 (hypercapnia) leads to an increase in the rate and depth of respiration through activation of the chemoreceptor reflex. Chemoreceptor activity, however, also affects cardiovascular function either directly (by interacting with medullary vasomotor centers) or indirectly (via altered pulmonary stretch receptor activity). Impaired gas exchange in the lungs, which can be caused by hypoventilation, respiratory arrest, pulmonary edema, pulmonary embolism, etc., decreases arterial PO2 and pH, and increases arterial PCO2. These changes stimulate chemoreceptor activity leading to enhanced sympathetic outflow to the heart and vasculature via activation of the rostral ventrolateral medulla. Cerebral ischemia activates central chemoreceptors in a manner that produces simultaneous activation of sympathetic and vagal nerves to the cardiovascular system.
The carotid bodies are located on the external carotid arteries near their bifurcation with the internal carotids. Each carotid body is a few millimeters in size and has the distinction of having the highest blood flow per tissue weight of any organ in the body. Afferent nerve fibers join with the sinus nerve before entering the glossopharyngeal nerve. Hypoxemia, hypercapnia and acidosis lead to an increase in carotid body receptor firing. When hypoxemia results in a PO2 lower than about 80 mmHg (threshold PO2), receptor firing is stimulated (normal arterial PO2 is about 95 mmHg). Any elevation of PCO2 above a normal value of 40 mmHg, or a decrease in pH below 7.4 causes receptor firing. If respiratory activity is not allowed to change during chemoreceptor stimulation (thus removing the influence of lung mechanoreceptors), then chemoreceptor activation causes bradycardia and coronary vasodilation (both via vagal activation) and systemic vasoconstriction (via sympathetic activation). If respiratory activity increases in response to the chemoreceptor reflex, then increased sympathetic activity stimulates both the heart and vasculature to increase arterial pressure. A decrease in carotid body blood flow as can occur during circulatory shock also increases receptor firing.