The sensitivity of the carotid sinus reflex can be changed. The application of norepinephrine locally or stimulation of sympathetic nerve fibers to the carotid sinuses enhances the receptors' sensitivity, resulting in a greater depressor response when there is an increase in intrasinus pressure. Hypertension causes a decrease in baroreceptor sensitivity because the carotid sinuses become stiffer due to the high intra-arterial pressure. As a result, a given increase in carotid sinus pressure leads to a smaller decrease in systemic arterial pressure compared to normal blood pressure levels. This raises the set point of the baroreceptors in hypertension, increasing the threshold and reducing the pressure receptors' sensitivity to changes in transmural pressure. Denervation of the carotid sinus can lead to temporary or prolonged hypertension.

The arterial baroreceptors play a crucial role in short-term adjustments of blood pressure in response to sudden changes in blood volume, cardiac output, or peripheral resistance, such as during exercise. However, long-term control of blood pressure over days or weeks depends on the individual's fluid balance, specifically the balance between fluid intake and output. The kidney is the most important organ in controlling body fluid volume and, consequently, blood pressure.

Cardiopulmonary receptors are found in the atria, ventricles, and pulmonary vessels. These baroreceptors are innervated by vagal and sympathetic afferent nerves. Cardiopulmonary reflexes are continuously active and can alter peripheral resistance in response to changes in intracardiac, venous, or pulmonary vascular pressure.

There are two types of cardiopulmonary baroreceptors in the atria: type A receptors activated by tension during atrial systole, and type B receptors activated by atrial diastole stretch. Stimulation of these atrial receptors sends impulses through vagal fibers to the vagal center in the medulla. As a result, sympathetic activity decreases in the kidney while increasing in the sinus node. These changes in sympathetic activity lead to increased renal blood flow, urine flow, and heart rate.

Activation of cardiopulmonary receptors can also trigger a reflex that lowers arterial blood pressure by inhibiting the vasoconstrictor center in the cerebral medulla. Stimulation of these receptors inhibits the release of angiotensin, aldosterone, and vasopressin (antidiuretic hormone). Disruption of the reflex pathway has the opposite effects.

The role of activation of these baroreceptors in regulating blood volume becomes evident in the body's response to hemorrhage. A reduction in blood volume (hypovolemia) enhances sympathetic vasoconstriction in the kidney and increases the secretion of renin, angiotensin, aldosterone, and vasopressin. Renal vasoconstriction, primarily affecting afferent arterioles, reduces glomerular filtration and stimulates the release of renin from the kidney. Renin acts on a plasma substrate to produce angiotensin II, which stimulates aldosterone secretion from the adrenal cortex. Increased vasopressin release decreases renal water excretion, while aldosterone release reduces renal NaCl excretion. These actions cause the kidneys to retain salt and water, leading to an increase in blood volume. Angiotensin II also elevates systemic arteriolar tone.

In some individuals, the carotid sinus is abnormally sensitive to external pressure. Consequently, tight collars or other forms of external pressure applied over the carotid sinus region may cause marked hypotension and fainting. This hypersensitivity is known as the carotid sinus syndrome.
In addition, the sensitivity of the carotid sinus reflex can be altered. Local application of norepinephrine or stimulation of sympathetic nerve fibers to the carotid sinuses enhances the sensitivity of its receptors in such a way that a given increase in intrasinus pressure produces a greater depressor response. Baroreceptor sensitivity decreases in hypertension because the carotid sinuses become stiffer as a result of the high intra-arterial pressure. Consequently, a given increase in carotid sinus pressure elicits a smaller decrease in systemic arterial pressure than it does at a normal level of blood pressure. Thus the set point of the baroreceptors is raised in hypertension in such a way that the threshold is increased and the pressure receptors are less sensitive to changes in transmural pressure. As would be expected, denervation of the carotid sinus can produce temporary and, in some instances, prolonged hypertension.
The arterial baroreceptors play a key role in short-term adjustments in blood pressure in response to relatively abrupt changes in blood volume, cardiac output, or peripheral resistance (as in exercise). However, long-term control of blood pressure—over a period of days or weeks—is determined by the fluid balance of the individual: namely, the balance between fluid intake and fluid output. By far, the most important organ in the control of body fluid volume, and hence blood pressure, is the kidney (see also
Cardiopulmonary receptors are located in the atria, ventricles, and pulmonary vessels. These baroreceptors are innervated by vagal and sympathetic afferent nerves. Cardiopulmonary reflexes are tonically active and can alter peripheral resistance in response to changes in intracardiac, venous, or pulmonary vascular pressure.
The atria contain two types of cardiopulmonary baroreceptors: those activated by the tension developed during atrial systole (type A receptors) and those activated by ofmeanarterialpressure.stretch of the atria during atrial diastole (type B receptors).
Stimulation of these atrial receptors sends impulses up vagal fibers to the vagal center in the medulla. Consequently, sympathetic activity is decreased to the kidney and increased to the sinus node. These changes in sympathetic activity increase renal blood flow, urine flow, and heart rate.
Activation of the cardiopulmonary receptors can also initiate a reflex that lowers arterial blood pressure by inhibiting the vasoconstrictor center in the cerebral medulla. Stimulation of the cardiopulmonary receptors inhibits release of angiotensin, aldosterone, and vasopressin (antidiuretic hormone); interruption of the reflex pathway has the opposite effects.
The role that activation of these baroreceptors plays in the regulation of blood volume is apparent in the body’s responses to hemorrhage. The reduction in blood volume (hypovolemia) enhances sympathetic vasoconstriction in the kidney and increases the secretion of renin, angiotensin, aldosterone, and vasopressin (see also ). The renal vasoconstriction (primarily afferent arterioles) reduces glomerular filtration and increases release of renin from the kidney. Renin acts on a plasma substrate to yield angiotensin II, which stimulates aldosterone secretion by the adrenal cortex. The enhanced release of vasopressin decreases renal water excretion, and the release of aldosterone decreases renal NaCl excretion. The kidneys retain salt and water, and hence blood volume increases. Angiotensin II (formed from angiotensin I by angiotensin-converting enzyme) also raises systemic arteriolar tone (see
Table 14.1
Insomeindividuals,thecarotidsinusisabnormallysensitivetoexternalpressure.Hence,tightcollarsorotherformsofexternalpressureovertheregionofthecarotidsinusmayelicitmarkedhypotensionandfainting.Suchhypersensitivityisknownasthecarotid sinus syndrome.