Peripheral chemoreceptors are small, highly vascular bodies located near the aortic arch (aortic bodies) and just medial to the carotid sinuses (carotid bodies). These vascular bodies are sensitive to changes in the oxygen levels (PO2), carbon dioxide levels (PCO2), and acidity (pH) of arterial blood. Their primary function is to regulate respiration, but they also have an impact on the vasomotor regions. When there is a decrease in the oxygen levels in the blood (PaO2), the chemoreceptors are stimulated. This increased activity in the afferent nerve fibers from the carotid and aortic bodies stimulates the vasoconstrictor regions, resulting in an increase in resistance and capacitance vessel tone.

The chemoreceptors are also stimulated by an increase in the carbon dioxide levels in arterial blood (PaCO2) and a decrease in pH. However, the reflex effect is not as significant as the direct effects of high carbon dioxide levels (hypercapnia) and acidosis on the vasomotor regions in the medulla. When hypoxia and hypercapnia occur together, the chemoreceptors have a greater impact than the combined effects of each stimulus alone.

In addition to the aortic and carotid bodies, chemoreceptors are also found in the heart. These cardiac chemoreceptors are activated when there is insufficient blood supply to the heart muscle, leading to precordial pain known as angina pectoris.

The optimal functioning of cardiovascular reflexes relies on the integrity of the pontine and hypothalamic structures. These structures are responsible for both the behavioral and emotional control of the cardiovascular system. Stimulation of the anterior hypothalamus causes a decrease in blood pressure and a slower heart rate, while stimulation of the posterolateral region of the hypothalamus increases both blood pressure and heart rate. The hypothalamus also contains a temperature-regulating center that affects blood vessels in the skin. Cold stimuli cause constriction of skin vessels, conserving heat, while warm stimuli cause cutaneous vasodilation and enhanced heat loss.

The cerebral cortex also plays a role in regulating blood flow distribution in the body. Stimulation of the motor and premotor areas usually leads to an increase in blood pressure, known as a pressor response. However, emotional stimuli can evoke vasodilation and depressor responses, such as blushing or fainting.

Painful stimuli can elicit either pressor or depressor responses, depending on the intensity and location of the stimulus. Distention of the viscera often leads to a depressor response, while painful stimuli to the body surface typically result in a pressor response.

The inflation of the lungs triggers a reflex that causes systemic vasodilation and a decrease in arterial blood pressure. Conversely, lung collapse induces systemic vasoconstriction. The afferent fibers responsible for mediating this reflex are found in the vagus nerves and possibly the sympathetic nerves. Stimulation of these fibers by lung stretch inhibits the vasomotor areas. The magnitude of the depressor response to lung inflation depends on the degree of inflation and the existing level of vasoconstrictor tone.

Increases in carbon dioxide levels stimulate the chemosensitive regions of the medulla (central chemoreceptors), leading to vasoconstriction and increased peripheral resistance. Decreasing carbon dioxide levels through hyperventilation reduces the tonic activity in these medullary areas and, consequently, decreases peripheral resistance. The chemosensitive regions in the medulla are also influenced by changes in pH. Lowering of blood pH stimulates these cerebral areas, while an increase in blood pH inhibits them. These effects may be mediated through changes in cerebrospinal fluid pH, similarly to the respiratory center.
Peripheral chemoreceptors consist of small, highly vascular bodies in the region of the aortic arch (aortic bodies; see
Fig. 18.26 ) and just medial to the carotid sinuses (carotid bodies; see
Fig. 18.25 ). These vascular bodies are sensitive to changes in the PO2, PCO2, and pH of arterial blood. Although they primarily regulate respiration, they also influence the vasomotor regions. A reduction in PaO2 stimulates the chemoreceptors. The increased activity in afferent nerve fibers from the carotid and aortic bodies stimulates the vasoconstrictor regions and thereby increases the tone of resistance and capacitance vessels.
The chemoreceptors are also stimulated by increased arterial blood PCO2 (PaCO2) and by reduced pH. However, the reflex effect is small in comparison to the direct effects of hypercapnia (high PaCO2) and acidosis on the vasomotor regions in the medulla. When hypoxia and hypercapnia occur simultaneously, the effects of the chemoreceptors are greater than the sum of the effects of each of the two stimuli when they act alone.
Chemoreceptors are also located in the heart. These cardiac chemoreceptors are activated by ischemia of cardiac muscle, and they transmit the precordial pain (angina pectoris) associated with an inadequate blood supply to the myocardium.
Optimal function of the cardiovascular reflexes requires integrity of the pontine and hypothalamic structures. Furthermore, these structures are responsible for behavioral and emotional control of the cardiovascular system (see also ). Stimulation of the anterior hypothalamus produces both a fall in blood pressure and bradycardia, whereas stimulation of the posterolateral region of the hypothalamus increases both blood pressure and the heart rate. The hypothalamus also contains a temperature-regulating center that affects blood vessels in the skin. Stimulation by the application of cold to the skin or by cooling of the blood perfusing the hypothalamus results in constriction of the skin vessels and heat conservation, whereas warm stimuli to the skin result in cutaneous vasodilation and enhanced heat loss.
The cerebral cortex also affects blood flow distribution in the body. Stimulation of the motor and premotor areas affects blood pressure; usually, a pressor response occurs. However, vasodilation and depressor responses may be evoked, as in blushing or fainting, in response to an emotional stimulus.
Painful stimuli can elicit either pressor or depressor responses, depending on the magnitude and location of the stimulus. Distention of the viscera often evokes a depressor response, whereas painful stimuli to the body surface generally evoke a pressor response.
Inflation of the lungs initiates a reflex that induces systemic vasodilation and a decrease in arterial blood pressure. Conversely, collapse of the lungs evokes systemic vasoconstriction. Afferent fibers that mediate this reflex are in the vagus nerves and possibly also in the sympathetic nerves. Stimulation of these fibers by stretch of the lungs inhibits the vasomotor areas. The magnitude of the depressor response to lung inflation is directly related to the degree of inflation and to the existing level of vasoconstrictor tone (see also
Increases in PCO2 stimulate chemosensitive regions of the medulla (the central chemoreceptors), and they elicit vasoconstriction and increased peripheral resistance. A reduction in PCO2 to subnormal levels (in response to hyperventilation) decreases tonic activity in these areas in the medulla and thereby decreases peripheral resistance. The chemosensitive regions are also affected by changes in pH. Lowering of blood pH stimulates these cerebral areas, and a rise in blood pH inhibits them. These effects of changes in PCO2 and blood pH may operate through changes in cerebrospinal fluid pH, as may also the respiratory center.