Regulation of the mean arterial pressure

Regulation of the mean arterial pressure: The mean arterial pressure is on average maintained around 100 mmhg. It is derived as a product of cardiac output and total peripheral resistance or from the diastolic and pulse pressures. It is essential to maintain the mean arterial pressure to preserve adequate tissue perfusion and oxygenation. It is regulated by several neurohormonal mechanisms and by the brainstem cardiovascular center which regulates autonomic nervous system activity depending on the information it receives from end organs like baroreceptors and chemoreceptors.

1. Brainstem cardiovascular center: It 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 which synapses with sympathetic neurons in the intermediolateral columns in the spinal cord, sympathetic ganglia and ultimately to blood vessels. It promotes vasoconstriction of the arterioles and venules and is important in maintaining resting tone of the blood vessels. The cardiac accelerator center also forms a part of the sympathetic outflow. The end organ innervated is the heart. Stimulation causes increased contractility, increased heart rate and increased conduction velocity i.e. effects of sympathetic stimulation of the heart. The cardiac decelerator center forms the central parasympathetic outflow. It innervates and inhibits the SA node to decrease heart rate.

2. Baroreceptor reflex: Baroreceptors are mechanoreceptors that respond to stretch on 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. The baroreceptors in the carotid sinus are innervated by the glossopharyngeal nerve (IX) through the Herring’s nerve while those in the aortic arch are innervated by the vagus nerve (X). Afferents from the baroreceptors will synapse in the brainstem in the nucleus tractus solitarius which in turn influences the cardiovascular center. Baroreceptors are involved in the short term regulation of blood pressure only. The aortic arch baroreceptors are less sensitive and respond at higher pressures compared to the carotid sinus receptors. The carotid sinus baroreceptors will respond to increase or decrease in blood pressure while the aortic baroreceptors will respond only to increase in blood pressure. Overall, the baroreceptors are more sensitive to changes in blood pressure.

Decrease in blood pressure can happen physiologically with postural changes like standing up from a sitting or lying down position or pathologically in blood loss from hemorrhage. Valsalva maneuver, which involves 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, the 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 increase and decrease in blood pressure.

*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.

3. Other factors affecting the MAP: Changes in the diameter of blood vessels as seen in atherosclerosis, arteriosclerosis, local tissue metabolic changes with changes in nitric oxide, adenosine, H+, K+, histamine, endothelins and prostacyclins can affect the TPR and hence the MAP.

   Low pressure baroreceptors or 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 the low pressure baroreceptors causing a decrease in the secretion of ADH, renin and aldosterone and increased secretion of ANP.

   Peripheral chemoreceptors in the aortic and carotid bodies and central chemoreceptors detect changes in arterial oxygenation levels. They activate the central sympathetic outflow in response to hypoxia, hypercarbia and acidosis causing intense peripheral vasoconstriction, increased TPR and increased blood pressure. The peripheral chemoreceptors may cause bradycardia initially by activating the parasympathetic outflow to the heart but it is superseded by hyperventilation that decreases the parasympathetic outflow, ultimately increasing the heart rate.