Regulation of the mean arterial pressure: Mean arterial pressure (MAP) is maintained at about 100 mmHg. You can estimate it as the product of cardiac output (CO) and total peripheral resistance (TPR), or derive it from the diastolic pressure and pulse pressure. Maintaining MAP is essential for adequate tissue perfusion and oxygen delivery.
MAP is regulated by several neurohormonal mechanisms. A key controller is the brainstem cardiovascular center, which adjusts autonomic nervous system activity based on input from end organs such as baroreceptors and chemoreceptors.
Brainstem cardiovascular center: This center is located in the medulla and lower pons. It has three components: the vasoconstrictor center, the cardiac accelerator center, and the cardiac decelerator center.
The vasoconstrictor center is part of the central sympathetic outflow. It synapses with sympathetic neurons in the intermediolateral columns of the spinal cord, then in sympathetic ganglia, and ultimately reaches blood vessels. It promotes vasoconstriction of arterioles and venules and is important for maintaining the resting tone of blood vessels.
The cardiac accelerator center is also part of the sympathetic outflow. Its end organ is the heart. Stimulation increases contractility, increases heart rate, and increases conduction velocity (the typical effects of sympathetic stimulation of the heart).
The cardiac decelerator center forms the central parasympathetic outflow. It innervates and inhibits the SA node, decreasing heart rate.
Baroreceptor reflex: Baroreceptors are mechanoreceptors that respond to stretch in the arterial wall. They are located in the carotid sinus (at the bifurcation of the external and internal carotid arteries) and in the aortic arch.
Afferent signals from baroreceptors synapse in the brainstem at the nucleus tractus solitarius, which then influences the cardiovascular center.
Baroreceptors are involved in short term regulation of blood pressure only. Aortic arch baroreceptors are less sensitive and respond at higher pressures than carotid sinus receptors. Carotid sinus baroreceptors respond to both increases and decreases in blood pressure, while aortic baroreceptors respond only to increases in blood pressure. Overall, baroreceptors are highly sensitive to changes in blood pressure.
A decrease in blood pressure can occur physiologically with postural changes (for example, standing up from sitting or lying down) or pathologically with blood loss from hemorrhage. The Valsalva maneuver (expiring against a closed glottis) reduces venous return to the heart and activates the baroreceptor reflex to increase blood pressure and heart rate.
In chronic hypertension, baroreceptors become less sensitive, and the blood pressure set point in the cardiovascular center is higher than normal.
The following table shows the baroreceptor reflex in response to increases and decreases in blood pressure.
| Increase in blood pressure | Decrease in blood pressure |
| Increased stretch on baroreceptors | Decreased stretch on baroreceptors |
| Increased firing in afferent nerves | Decreased firing in afferent nerves |
| Increased parasympathetic activity | Decreased parasympathetic activity |
| Decreased sympathetic activity | Increased sympathetic activity |
| Heart rate decreases | Heart rate increases |
| Decreased contractility | Increased contractility |
| Cardiac output decreases | Cardiac output increases |
| Decreased TPR | Increased TPR |
| Unstressed volume increases* | Stressed volume increases** |
*unstressed volume is the blood volume contained in the veins
**stressed volume is the blood volume contained in the arteries
The renin-angiotensin aldosterone system is important for long term regulation of blood pressure.
Other factors affecting the MAP: Changes in the diameter of blood vessels (as seen in atherosclerosis and arteriosclerosis) can affect TPR and therefore MAP. Local tissue metabolic changes can also alter vascular tone through mediators such as nitric oxide, adenosine, H+, K+, histamine, endothelins, and prostacyclins.
Low pressure baroreceptors (volume receptors) are present in the large veins, pulmonary arteries, atria, and ventricles. They respond to changes in blood volume. Increased blood volume increases stretch on these receptors, leading to decreased secretion of ADH, renin, and aldosterone, and increased secretion of ANP.
Peripheral chemoreceptors in the aortic and carotid bodies, along with central chemoreceptors, detect changes in arterial oxygenation. In response to hypoxia, hypercarbia, and acidosis, they activate the central sympathetic outflow, causing intense peripheral vasoconstriction, increased TPR, and increased blood pressure. Peripheral chemoreceptors may initially cause bradycardia by activating parasympathetic outflow to the heart, but this effect is superseded by hyperventilation, which decreases parasympathetic outflow and ultimately increases heart rate.
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