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 the 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 peripheral chemoreceptors are found in carotid bodies on the external carotid arteries near their bifurcation with the internal carotids. Afferent nerve fibers from the carotid bodies join with the sinus nerve before entering the glossopharyngeal nerve (cranial nerve IX) and travelling up to the nucleus tractus solitarius (NTS) in the medulla. Aortic body chemoreceptors are found scattered along the aortic arch and innervated by the vagus nerve (cranial nerve X). Because the carotid bodies have discrete locations on each external carotid, they have been studied the most. 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; this high flow is associated with a high cellular oxygen consumption. Because of this feature, a decrease in carotid body blood flow as can occur during circulatory shock also increases receptor firing by decreasing carotid body blood flow and producing a condition referred to as "stagnant hypoxia."
Although hypoxemia is a primary stimulus for carotid body receptors, hypercapnia and acidosis also stimulate the carotid body. As arterial blood PO2 decreases below its normal value of about 95 mmHg, there is a progressive increase in receptor firing rate. Any elevation of PCO2 above a normal value of 40 mmHg, or a decrease in pH below 7.4, enhances receptor firing at a given PO2. The cardiovascular response to arterial chemoreceptor activation is determined, in part, by the respiratory response. If respiratory activity prevented from changing during chemoreceptor stimulation (thus removing the influence of lung mechanoreceptors), then chemoreceptor activation of the carotid bodies 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.