Arterial Pressure Regulation

5/12/23, 0:17 Arterial Pressure Regulation - United Arab Emirates University
Arterial Pressure Regulation

Mean arterial pressure (MAP) is the average systemic pressure in the arteries. The MAP
is tightly regulated to help maintain appropriate perfusion and is primarily determined
by the cardiac output (CO) and the systemic vascular resistance (SVR). Cardiac output
is determined by the HR and the stroke volume (the volume of blood ejected by the
heart each beat). The HR is primarily regulated by the effects of the ANS on the
sinoatrial node in the heart, while stroke volume is determined by the preload,
afterload, and inotropy (or contractile strength) of each heartbeat. The SVR is regulated
by a number of factors, including the ANS, the arterial baroreflex, circulating
catecholamines, the RAAS, and several other hormones.
Last updated: March 21, 2023
CONTENTS
Overview
Regulation by the ANS
Arterial Baroreceptor Reflex
Renin-Angiotensin-Aldosterone System (RAAS)
Other Hormones Involved in Arterial Pressure Regulation
Clinical Relevance
References
Overview
https://uaeu.lecturio.com/#/article/3892?return=__app__%2Fsearch%2Fconcepts%2FRegulation%2520of%2520blood%2520pressure 1/18
Mean arterial pressure (MAP) equations

Mean arterial pressure is the average systemic arterial pressure.
MAP = (CO x SVR) + CVP

CO: cardiac output, which = stroke volume x HR
SVR: systemic vascular resistance
CVP: central venous pressure (close to 0, often disregarded)
Can be approximated using systolic and diastolic blood
pressures:
Because the heart spends more time in diastole than in
systole, the diastolic blood pressure (DBP) contributes more
to the MAP than the systolic blood pressure (SBP).
Equation: MAP ≅ [ ⅓ (SBP ‒ DBP) ] + DBP
Mean arterial intravascular pressure throughout the cardiac cycle

P: pressure
Image by Lecturio.
Factors affecting the mean arterial pressure

Mean arterial pressure is primarily affected by the CO and SVR:
CO = HR x stroke volume:
HR is determined by:
ANS (primary regulator) effects on the sinoatrial node in the
heart
Other factors:
Thyroid hormones
Circulating catecholamines
K+ levels
Ischemia
Stroke volume is affected by:
Inotropy: contractile strength of each heartbeat
Afterload:
Pressure the left ventricle needs to overcome to eject
blood into the aorta
Closely related to SVR
Preload (how much the ventricles have stretched/filled with
blood by the end of diastole), which is affected by:
Venous compliance (how much blood the veins can
hold)
Blood volume, primarily affected by renal Na+ and H2O
handling
Systemic vascular resistance is primarily affected by:
Vascular anatomy:
Arrangement of vessels in series or parallel
Anatomy of the vessel walls
Local factors secreted by vessel walls (e.g., NO, prostacyclin,
thromboxane), which can cause vasoconstriction and vasodilation
Neuronal factors:
Input from the ANS
Arterial baroreceptor reflex
Hormones:
Circulating catecholamines released by the adrenal medulla
Hormones in the RAAS
Natriuretic peptides
Antidiuretic hormone (ADH)
Factors that affect mean arterial pressure (MAP).

CO: cardiac output
Image by Lecturio.
Regulation by the ANS

Sympathetic stimulation
Sympathetic stimulation increases MAP, which increases both SVR and CO:
↑ SVR by inducing vasoconstriction:

Via α1-adrenergic receptors, which are coupled to Gq
proteins
Uses inositol trisphosphate (IP3) signal transduction →
contracts smooth muscle
↑ CO by increasing both HR and stroke volume
Directly, via β1-adrenergic receptors, which increases:
Contractility (leading to ↑ stroke volume)
cAMP → ↑ rate of depolarization at the sinoatrial (SA)
node) → ↑ HR
By inducing venoconstriction → forces more blood back to
the heart → ↑ preload → ↑ stroke volume → ↑ CO
By ↑ blood volume through activation of the RAAS → ↑
preload → ↑ stroke volume → ↑ CO
Parasympathetic stimulation
Parasympathetic stimulation decreases MAP by decreasing both SVR and CO:
↓ SVR by inducing vasodilation

↓ CO by decreasing HR
Via muscarinic M2 receptors which are coupled to Gi
proteins
Leads to ↓ cAMP → ↓ rate of depolarization at the SA node
→ ↓ HR
Regions of autonomic output regulation

Hypothalamus: regulates “automatic” ANS output
Medulla: coordinates baroreceptor reflex responses (see below)
Cerebral cortex: adjusts ANS output based on cognitive thought
processes (i.e., fear, stress, relaxation)
Spinal cord: contains sympathetic efferents under reflexive
control of the spinal cord
Arterial Baroreceptor Reflex

The baroreceptor reflex is the most important mechanism for acute BP regulation.
Baroreceptors
Pressure-sensing neurons
Fire continuously, though firing rate varies depending on the
blood pressure
Location of baroreceptors:
Carotid sinus:
Located where the common carotids divide into their
internal and external branches
Innervated by the glossopharyngeal nerve (cranial nerve
(CN) IX) nerve
Aortic arch: innervated by the vagus nerve (CN X)
Locations of the carotid and aortic baroreceptors

Image by Lecturio.
Baroreceptor reflex
↑ Blood pressure or blood volume → ↑ vessel stretching

Baroreceptor nerves ↑ firing frequency when they sense ↑ stretch
Respond in milliseconds
Firing rate changes between systole and diastole of a single
heartbeat
Signal sent through afferent fibers → nucleus tractus solitarius in
the medulla
Appropriate response is coordinated in the cardiovascular control
centers of the medulla and sent out via ANS fibers
3 primary output centers in the cardiovascular control center:
Sympathetic centers:
Cardioacceleratory center: ↑ HR and inotropy when
activated
Vasomotor center: ↓ preload and SVR when activated
Vagal/parasympathetic center:
Cardioinhibitory center: ↓ HR when activated
Baroreceptors are neurons that sense the stretching of a blood vessel.

P: pressure
Image by Lecturio.
Example: ↑ blood pressure

↑ Blood pressure → ↑ vessel stretch → ↑ rate of baroreceptor firing → leads to:
Activation of the vagal/parasympathetic center (i.e.,

cardioinhibitory center): ↓ HR
Inhibition of the sympathetic centers (i.e., cardioacceleratory and
vasomotor centers):
↓ Inotropy
Venodilation → ↓ preload → ↓ stroke volume → ↓ CO
Vasodilation → ↓ SVR
End effect = ↓ blood pressure
Responses of the baroreceptor reflex to increased blood pressure:

HR: heart rate
CO: cardiac output
Image by Lecturio.
Example: ↓ blood pressure (that is,

hypotension)
↓ Blood pressure → ↓ stretch → ↓ rate of baroreceptor firing → leads to:
Inhibition of the vagal/parasympathetic center (i.e.,

cardioinhibitory center): ↑ HR
Activation of the sympathetic centers (i.e., cardioacceleratory and
vasomotor centers):
↑ Inotropy
Venoconstriction → ↑ preload → ↑ stroke volume → ↑ CO
Vasoconstriction → ↑ SVR
End effect = ↑ blood pressure
Responses of the baroreceptor reflex to decreased blood pressure:

HR: heart rate
CO: cardiac output
Image by Lecturio.
Adjusting baroreceptor function
Baroreceptors are rapidly adapting → involved only in short-term

(i.e., second to second) blood pressure regulation
Even if baseline blood pressure range is chronically elevated
(or lowered), the body still needs to be able to make short-
term adjustments to maintain appropriate blood pressure
during normal activities (e.g., standing up, walking up stairs).
Certain situations require the normal range for baroreceptor
firing to be “reset” or adjusted .
The baroreceptor reflex follows a sigmoidal curve:
Arterial pressure plotted on the x-axis
Baroreceptor firing frequency plotted on the y-axis
Highest rate of firing is during the steepest part of the curve
Effects of chronically elevated blood pressure (e.g., chronic
hypertension)
Shifts the curve to the right
Baroreceptors do not increase firing rate until higher levels
of stretch are sensed.
Other situations in which baroreflex set point is adjusted for
shorter periods of time:
Aerobic exercise
Pain
Relationship between arterial pressure and baroreceptor firing frequency in

normotensive and hypertensive patients:
As arterial pressure increases, the baroreceptor afferent neurons fire more
frequently in a sigmoidal relationship. Chronic hypertension decreases the
sensitivity of the baroreceptors, shifting the curve to the right.
MAP: mean arterial pressure
Image by Lecturio.
Renin-Angiotensin-Aldosterone
System (RAAS)
The RAAS is the major long-term regulator of blood pressure.
Enzymes and hormones in the RAAS
Renin:
Secreted by the macula densa cells within the kidneys
Converts angiotensinogen (secreted by hepatocytes) to
angiotensin I
ACE:
Secreted by pulmonary vascular endothelium
Converts angiotensin I to angiotensin II
Angiotensin II:
Stimulates release of aldosterone (secreted by the
zona glomerulosa in the adrenal cortex)
↑ ADH secretion → ↑ renal reabsorption of water
↑ Thirst
↓ Venous compliance through angiotensin type 1 (AT1)
receptors
Aldosterone:
Stimulates Na+ and water reabsorption from the renal tubules
Stimulates excretion of K+ and H+ into the urine
Stimulation of RAAS
Factors that stimulate the RAAS (i.e., renin secretion) include:
↓ Renal perfusion:
↓ Blood pressure
↓ Effective circulating blood volume
↓ Sodium delivery to the kidney
↑ Sympathetic stimulation
End results of RAAS activation

Renin → angiotensin I → angiotensin II → aldosterone:
↑ BP: induces reabsorption of water and Na+, leading to ↑ blood

volume → ↑ preload → ↑ stroke volume → ↑ CO → ↑ MAP
↑ Serum Na+ (by ↓ urinary excretion of Na+)
↓ Serum K+ (by ↑ urinary excretion of K+)
↑ Serum pH (by ↑ urinary excretion of H+)
Renin-angiotensin-aldosterone system:
A decrease in mean arterial pressure (MAP) is sensed by the juxtaglomerular
apparatus, which then secretes renin. Renin catalyzes the synthesis of
angiotensin I which is converted into angiotensin II by ACE. Angiotensin II
induces the release of aldosterone from the adrenal cortex, which travels to
the distal convoluted tubule, where it causes reabsorption of Na+ and water.
CO: cardiac output
Image by Lecturio.
Other Hormones Involved in

Arterial Pressure Regulation
Circulating catecholamines
Circulating catecholamines are secreted by the adrenal medulla

directly into the bloodstream
Catecholamine hormones:
Epinephrine (80%)
Norepinephrine (20%)
Effects of catecholamines that ↑ blood pressure:
Via cardiac β1-adrenergic receptors → ↑ HR and ↑
stroke volume
Via renal β1-adrenergic receptors → ↑ RAAS → ↑ blood
volume
Via blood vessel α1 receptors → vasoconstriction
Other effects of catecholamines:
↑ Respirations and bronchodilation
↑ Blood glucose levels
↓ Digestion
Circulating catecholamines are ↑ by:
Physical activity
Stress
Heart failure
Shock
Pheochromocytoma
Natriuretic peptides
These hormones act in opposition to the RAAS.
2 types of natriuretic peptides:

Atrial natriuretic peptide (ANP): stored in and released by
atrial myocytes
Brain-type natriuretic peptide (BNP):
Stored in and released by ventricular myocytes
Diagnostic marker for heart failure
ANP and BNP have similar actions:
↓ Renin release → ↓ angiotensin II → ↓ aldosterone →
diuresis (water loss) and natriuresis (Na+ loss) → ↓ blood
volume → ↓ preload → ↓ CO → ↓ MAP
Minor effects which ↓ CVP and SVR
Released in response to:
Atrial distention (most important factor)
Angiotensin II
Endothelin
Effects of atrial natriuretic peptide (ANP) on blood volume:

Atrial natriuretic peptide is released by atrial myocytes in response to
distention and decreases the release of renin, which results in sodium loss
(natriuresis) and water loss (diuresis) in the urine. The loss of volume through
the urine decreases central venous pressure (CVP), preload, and systemic
vascular resistance (SVR), decreasing blood pressure.
GFR: glomerular filtration rate
NEP: neutral endopeptidase
Image by Lecturio.
Antidiuretic Hormone (ADH)

A neuropeptide secreted by the posterior pituitary

Also called vasopressin
Secreted in response to:
Angiotensin II
Hyperosmolarity
2 primary effects:
At typical levels:
Action is via vasopressin 2 (V2) receptors
Stimulates water reabsorption in the renal tubules and
collecting system (primary effect) → ↑ blood volume → ↑
preload → ↑ CO → ↑ MAP
At high levels: vasoconstriction via V1 receptors → ↑ SVR
Clinical Relevance
Hemorrhage: excessive blood loss that results in decreased

blood volume, leading to ↓ preload, ↓ stroke volume, ↓ CO, ↓ MAP,
and thus ↓ perfusion to vital organs. In order to maintain
perfusion, the body will compensate by attempting to increase
MAP by boosting CO through increases in HR and contractility,
and by vasoconstriction to increase systemic vascular resistance.
IV fluids and/or blood transfusions can help to restore blood
volume.
Fight-or-flight response: activation of the sympathetic
nervous system (SNS), which affects several aspects of the
cardiac cycle simultaneously. The SNS activation increases
contractility of the heart, while causing vasoconstriction and
increasing venous return to the heart. These conditions result in
synergistic effects, increasing stroke volume owing to effects on
both ↑ preload and ↑ inotropy.
States of low cardiac output, such as heart failure, liver cirrhosis
, and cor pulmonale from severe lung disease may cause
abnormally high stimulation of the RAAS in an attempt to maintain
adequate arterial pressures. The abnormally high aldosterone,
however, may lead to metabolic complications, such as
hypokalemia and/or metabolic alkalosis.
References
1. Mohrman, D. E., Heller, L. J. (2018). Overview of the cardiovascular system.

Chapter 1 of Cardiovascular physiology, 9th ed. McGraw-Hill Education.
accessmedicine.mhmedical.com/content.aspx?aid=1153946098
2. Mohrman, D. E., Heller, L. J. (2018). Vascular control. Chapter 7 of
Cardiovascular physiology, 9th ed. McGraw-Hill Education.
3. Mohrman, D. E., Heller, L. J. (2018). Regulation of arterial pressure. Chapter 9 of
Cardiovascular physiology, 9th ed. McGraw-Hill Education.
4. Baumann, B. M. (2016). Systemic hypertension. Chapter 57 of J. E. Tintinalli, J. S.
Stapczynski, O. J. Ma, D. M. Yealy, G. D. Meckler & D. M. Cline (Eds.), Tintinalli’s
Emergency Medicine: A Comprehensive Study Guide, 8th ed. McGraw-Hill
Education. accessmedicine.mhmedical.com/content.aspx?aid=1121496251
5. Klabunde R. E. (2021). Cardiovascular physiology concepts. Retrieved June 10,
2021, from https://www.cvphysiology.com/
6. Saladin, K.S., Miller, L. (2004). Anatomy and physiology, 3rd ed., pp. 753–760.
McGraw-Hill Education.

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5/12/23, 0:17 Arterial Pressure Regulation - United Arab Emirates University

Last updated: March 21, 2023

Mean arterial pressure (MAP) equations

MAP = (CO x SVR) + CVP

Mean arterial intravascular pressure throughout the cardiac cycle

Factors affecting the mean arterial pressure

Factors that affect mean arterial pressure (MAP).

Regulation by the ANS

↑ SVR by inducing vasoconstriction:

↓ SVR by inducing vasodilation

Regions of autonomic output regulation

Arterial Baroreceptor Reflex

Locations of the carotid and aortic baroreceptors

↑ Blood pressure or blood volume → ↑ vessel stretching

Baroreceptors are neurons that sense the stretching of a blood vessel.

Example: ↑ blood pressure

Activation of the vagal/parasympathetic center (i.e.,

Responses of the baroreceptor reflex to increased blood pressure:

Example: ↓ blood pressure (that is,

Inhibition of the vagal/parasympathetic center (i.e.,

Responses of the baroreceptor reflex to decreased blood pressure:

Adjusting baroreceptor function

Baroreceptors are rapidly adapting → involved only in short-term

Relationship between arterial pressure and baroreceptor firing frequency in

Enzymes and hormones in the RAAS

End results of RAAS activation

↑ BP: induces reabsorption of water and Na+, leading to ↑ blood

Other Hormones Involved in

Circulating catecholamines are secreted by the adrenal medulla

2 types of natriuretic peptides:

Effects of atrial natriuretic peptide (ANP) on blood volume:

Antidiuretic Hormone (ADH)

A neuropeptide secreted by the posterior pituitary

Hemorrhage: excessive blood loss that results in decreased

1. Mohrman, D. E., Heller, L. J. (2018). Overview of the cardiovascular system.

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