Physiology, Mean Arterial Pressure

Article Author:
Daniel DeMers
Article Editor:
Daliah Wachs
2/24/2019 1:19:31 PM
PubMed Link:
Physiology, Mean Arterial Pressure


The definition of mean arterial pressure (MAP) is the average arterial pressure throughout one cardiac cycle, systole, and diastole. MAP is influenced by cardiac output and systemic vascular resistance, each of which is under the influence of several variables. These will be discussed further under the Mechanism heading of this article.[1]

Cardiac output is calculated as the product of heart rate and stroke volume. The determination of stroke volume is by ventricular inotropy and preload. Preload is affected by blood volume and the compliance of veins. Increasing the blood volume increases the preload, increasing the stroke volume, and therefore increasing cardiac output. Afterload also affects the stroke volume in that an increase in afterload will decrease stroke volume. Heart rate is affected by the chronotropy, dromotropy, and lusitropy of the myocardium.

Systemic vascular resistance is determined primarily by the radius of the blood vessels. Decreasing the radius of the vessels increases vascular resistance. Increasing the radius of the vessels would have the opposite effect. Blood viscosity can also affect systemic vascular resistance. An increase in hematocrit will increase blood viscosity and increase systemic vascular resistance. Viscosity, however, is considered only to play a minor role in systemic vascular resistance.[2]

A common method used to estimate the MAP is the following formula:

  • MAP = DP + 1/3(SP – DP) or MAP = DP + 1/3(PP)

Where DP is the diastolic blood pressure, SP is the systolic blood pressure, and PP is the pulse pressure. This method is often more conducive to measuring MAP in most clinical settings as it offers a quick means of calculation if the blood pressure is known.

Issues of Concern

To perfuse vital organs requires the maintenance of a minimum MAP of 60 mmHg. If MAP drops below this point for an extended period, end-organ manifestations such as ischemia and infarction can occur. If the MAP drops significantly, blood will not be able to perfuse cerebral tissues, there will be a loss of consciousness, and neuronal death will quickly ensue.[3] The body has several protective mechanisms to regulate MAP and ensure that a sufficient level of perfusion is maintained for the function of all organs.


MAP regulation is on the cellular level through a complex interplay between the cardiovascular, renal, and autonomic nervous systems. The relationships of these involved systems to one another will be discussed in more detail under the Mechanism heading of this article.

Organ Systems Involved

The cardiovascular system determines the MAP through cardiac output and systemic vascular resistance. Cardiac output is regulated on the level of intravascular volume, preload, afterload, myocardial contractility, heart rate, and conduction velocity. Systemic vascular resistance regulation is via vasoconstriction and dilation.

The renal system affects MAP via the renin-angiotensin-aldosterone system; this is a cascade that ends in the release of aldosterone, which increases sodium reabsorption in the distal convoluted tubules of the kidneys and ultimately increases plasma volume.

The autonomic nervous system plays a role in regulating MAP via baroreceptors located in the carotid sinus and aortic arch. The autonomic nervous system can affect both cardiac output and systemic vascular resistance to maintain MAP in the ideal range.

The functions of the above organ systems in regulating MAP are discussed further under the Mechanism heading of this article.


MAP functions to perfuse blood to all the tissues of the body to keep them functional. Mechanisms are in place to ensure that the MAP remains at least 60 mmHg so that blood can effectively reach all tissues.


Alterations in systemic vascular resistance and cardiac output are responsible for changes in MAP.

The most influential variable in determining the systemic vascular resistance is the radius of the blood vessels themselves. The radius of these vessels is influenced both by local mediators and the autonomic nervous system. Endothelial cells lining the blood vessels produce and respond to vasoactive substances to either dilate or constrict the vessels depending on the body’s needs.

When MAP is elevated, shearing forces on the vessel walls induce synthesis of nitric oxide (NO) in endothelial cells. NO diffuses into vascular smooth muscle cells where it activates guanylyl cyclase and results in the dephosphorylation of GTP to cGMP. The cGMP acts as a second messenger within the cell, ultimately leading to smooth muscle relaxation and dilation of the vessel. Other vasodilating compounds produced locally are bradykinin and the various prostaglandins, which act through similar mechanisms to result in the relaxation of vascular smooth muscle.[4]

Endothelin is a local vasoactive compound that has the opposite effects as NO on vascular smooth muscle. A reduced MAP triggers the production of endothelin within the endothelial cells. Endothelin then diffuses into the vascular smooth muscle cells to bind the ET-1 receptor, a Gq-coupled receptor, resulting in the formation of IP3 and calcium release from the sarcoplasmic reticulum, which leads to smooth muscle contraction and constriction of the vessel.[5]

The autonomic nervous system also plays a vital role in regulating MAP via the baroreceptor reflex. The arterial baroreceptors found in the carotid sinus and aortic arch act through a negative feedback system to maintain the MAP in the ideal range. Baroreceptors communicate with the nucleus tractus solitarius in the medulla of the brainstem via the glossopharyngeal nerve (cranial nerve IX) in the carotid sinus and the vagus nerve (cranial nerve X) in the aortic arch. The nucleus tractus solitarius determines the sympathetic or parasympathetic tone to either raise or lower MAP according to the body’s needs.[6]

When MAP is elevated, increasing baroreceptor stimulation, the nucleus tractus solitarius decreases sympathetic output and increases parasympathetic output. The increase in parasympathetic tone will decrease myocardial chronotropy and dromotropy, with less pronounced effects on inotropy and lusitropy, via the effect of acetylcholine on M2 muscarinic receptors in the myocardium. M2 receptors are Gi-coupled, inhibiting adenylate cyclase and causing a decrease in cAMP levels within the cell. The result is a decrease in cardiac output and a subsequent decrease in MAP.

Conversely, when the MAP decreases, baroreceptor firing decreases and the nucleus tractus solitarius acts to reduce parasympathetic tone and increase sympathetic tone. The increase in sympathetic tone will increase myocardial chronotropy, dromotropy, inotropy, and lusitropy via the effect of epinephrine and norepinephrine on beta1 adrenergic receptors in the myocardium. Beta1 receptors are Gs-coupled, activating adenylate cyclase and causing an increase in cAMP levels within the cell. In addition to this, epinephrine and norepinephrine act on vascular smooth muscle cells via alpha1 adrenergic receptors to induce vasoconstriction of both arteries and veins. Alpha1 receptors are Gq-coupled and act via the same mechanism as the ET-1 receptor mentioned above. The combination of these events increases both cardiac output and systemic vascular resistance, effectively increasing MAP.

Increased sympathetic tone also occurs during exercise, severe hemorrhage, and in times of psychologic stress.

The renal system helps to maintain MAP primarily through the regulation of plasma volume, which directly affects cardiac output. A drop in renal perfusion triggers the release of renin, launching the renin-angiotensin-aldosterone cascade. Aldosterone acts on the distal convoluted renal tubules to increase sodium reabsorption and therefore increase water reuptake and plasma volume. Angiotensin II acts on the vasculature via the AT1 receptor to induce smooth muscle contraction, resulting in vasoconstriction. The AT1 receptor is Gq-coupled and works via the same mechanism as the ET-1 and alpha1 receptors mentioned above. Together these changes will increase both cardiac output and systemic vascular resistance to increase MAP.

Related Testing

The use of a sphygmomanometer is the standard way to measure both the systolic and diastolic blood pressures. Once these values are known, a MAP value can easily be determined. An oscillometric blood pressure device can also be used to measure MAP. Echocardiography can be used to evaluate the function of the myocardium further, determine the left ventricular ejection fraction, and cardiac output. Central venous catheters, placed in the right atrium, can be used to measure central venous pressure when necessary.

Clinical Significance

 On the opposite end of the spectrum, hypotension, persistently low blood pressure, can be life-threatening as well. When the MAP maintenance is inadequate, vital organs do not receive the required blood supply, hypotensive shock ensues, and organ failure quickly follows. Hypotension often results from severe bacteremia or hypovolemia. This condition can be treated pharmacologically with dopamine and other vasopressors.[7]


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