page sections

• introduction
• the physics of blood pressure
• local regulation
• sympathetic innervation
• circulating hormonal factors
• summary
• resources and references

see also:

• measuring blood pressure

Blood Pressure

last authored: Dec 2012, Laura Clademenos
last reviewed:

 

 

Introduction

Blood pressure is the force exerted by blood within blood vessels as a result of the pumping action of the heart.
 
An adequate blood pressure is necessary for blood to travel from the heart around the body. A blood pressure that is too low (hypotension) can lead to inadequate blood flow, or hypoperfusion, of critical organs. A blood pressure that is too high (hypertension) can, over time, have detrimental health effects on organs such as the heart (myocardial infarction), the brain (stroke, hemorrhage), and kidneys (renal failure).
 

Blood pressure values are measured in mmHg (millimeters of mercury, atomic symbol Hg). A blood pressure of 100 mmHg, for example, means that the force generated would push a column of mercury, against gravity, 100 mm vertically. Blood pressure readings are presented as a fraction. The systolic blood pressure, the numerator, is defined as the peak pressure during the cardiac cycle, i.e. when the ventricles are contracting. The diastolic blood pressure, the denominator, is the pressure when the ventricles are relaxed. For example, a blood pressure of 120/80 represents a systolic pressure of 120 mmHg and a diastolic pressure of 80 mm Hg.
 

If the vascular system were not distensible, each cardiac cycle would send blood through arteries only during systole, during ventricular contraction. However, since vessels have elastic properties, they stretch during systole and gradually return to their resting size during diastole. This reduces the pulse pressure (the difference between systolic and diastolic pressure) and allows for more constant flow through capillaries.
 
Arteries are not very compliant, seeing only modest increases in volume following increases in pressure. This gives them the name resistance vessels. Veins are able to accommodate a larger volume of blood than arteries. They have a higher compliance and thinner walls, allowing them to function as capacitance vessels (Andreoli et al, 2010).
 
Vessel compliance can decrease temporarily with smooth muscle contraction, and also with age. Hardened arteries will experience increased systolic pressure and decreased diastolic pressure, leading to decreased capillary flow.
 
 
Physiologically, blood pressure is related to the product of the cardiac output and total peripheral resistance (BP = CO x TPR).
●     Cardiac output is the amount of blood leaving the heart with each contraction
●     Total peripheral resistance is sum of the resistance of all the blood vessels in the systemic circulation. Resistance relates to length, radius and number of blood vessels, as well as the viscosity of blood.

 

Changes to CO and TPR, and therefore BP, are regulated by the autonomic nervous system, which consists of the sympathetic and parasympathetic nervous systems.. Increased activity of the sympathetic nervous system (SNS) results in increased cardiac output contraction of arterioles, which increases systemic resistance.
 
 
Regulation of cardiac output is described in detail here; the following information focuses on peripheral resistance.

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The Physics of Blood Pressure

Pouiseuille’s law explains the relationship between pressure and flow. When blood flows through a vessel, the resistance (R) to that flow is determined by the characteristics of the blood and the vessel, including viscosity, length (L), viscosity (n) and radius (r).           R ∝ Ln/r⁴
As fluid viscosity or tube length increases, resistance to blood flow increases proportionately. However, these tend to be constant in human physiology. This leaves vessel radius to allow adjustment of peripheral resistance, and as the equation describes, a change in radius has an leads to a large change in resistance. This variation principally occurs in the arterioles, where small changes to arteriolar radius can exert large effects in resistance and therefore flow to an organ.
 
Arteriolar resistance is controlled by three major mechanisms: local regulation, sympathetic innervation, and circulating hormonal factors.

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Local Regulation

Blood pressure is constant throughout the body, and regional blood flow is adjusted to provide more or less blood to certain tissues to meet functional needs. Arteriolar smooth muscle senses changes in blood flow direction through stretch receptors. This automatic regulation leads to changes in vessel radius directly. Local metabolic conditions also impact vessel radius, as increased cellular activity suggests increased demand for blood flow. Decreased oxygen, increased CO2, increased nitric oxide, decreased pH, increased [K+], or increased adenosine all represent increased metabolic activity and lead to vasodilation.

Inflammation also involves vasodilation in an effort to combat pathogens and speed healing, mediated by bradykinin and histamine. Conversely, serotonin is released by platelets to lead to vasoconstriction during tissue damage.
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Sympathetic Innervation

main article: sympathetic nervous system
Blood pressure is heavily influenced by neurally mediated baroreceptors - stretch-sensitive nerve endings that transmit afferent impulses to the central nervous system.  High pressure baroreceptors are found in the carotid artery (the carotid sinus) and the wall of the aorta (aortic arch). Low pressure baroreceptors are found in the right atria and pulmonary arteries.
 
In response to baroreceptor activation, a reflex sends signals back to the body through the SNS and PSNS efferents. Decreases in blood pressure, and therefore stretch, prompt signals to transmit to control centres in the medulla. Activation of the SNS leads to efferent neuronal signals to the heart and vasculature, resulting in increased heart rate and contractility (cardiac output) and total peripheral resistance. These signals are mediated by the neurotransmitter nor-epinephrine (nor-adrenaline). Sympathetic innervation of the adrenal gland leads to release of the related sympathetic hormone epinephrine (adrenaline). Together, these raise blood pressure.
 
Sympathetic (SNS) activity increases:

• heart rate and contractility
• arteriolar vasoconstriction (increased total peripheral resistance)
• venous vasoconstriction and increased venous return
• sodium and water retention in kidney
• renin release (see below)
• ADH release (see below)

 
Conversely, when blood pressure (mean arterial pressure) rises, stretch receptors sense the rise in arterial pressure and increase the firing rate from the baroreceptors. This information is sent to the medulla in the brain stem to cause a number of changes: efferent SNS outflow is inhibited while the PSNS efferent response is increased.
 
Atrial natriuretic peptide (ANP) is released by the muscle fibres of the cardiac atria. It is released in response to atrial stretch, which can occur with increased blood volume. ANP acts on the kidneys to decrease Na+ reabsorption by the collecting ducts and increase the glomerular filtration rate. This allows the kidney to excrete more salt and water, thereby acting to compensate for the excess blood volume. Compared to other regulators of blood pressure, ANP exerts a relatively minor effect (Guyton and Hall, 2006).
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Circulating Hormonal Factors

main article: RAAS system
The kidney plays an important role in volume regulation and therefore blood pressure control. Firstly, it controls how much fluid is excreted or retained, directly impacting total blood volume. Additionally, through the activation of the renin-angiotensin-aldosterone system (RAAS), it has the potential to change the resistance in the arterioles of the kidney and cause the release of powerful chemical mediators to change peripheral vascular resistance.
 
The juxtaglomerular apparatus is found on the afferent and efferent arterioles of the glomerulus. It is made up of 3 different types of cells: juxtaglomerular, macula densa, and mesangial. The juxtaglomerular cells are smooth muscle cells found on the afferent arteriole, and their function  is to secrete renin. Macula densa cells detect changes in sodium concentrations and send out local vasoconstrictors to decrease or increase blood flow to the kidney. The function of mesangial cells is not well understood, but they are thought to influence the RAAS in coordination with the 2 other types of cells.
 

 

 

 

Renin is the enzyme released by the kidneys in response to these signals. By activating the RAAS, its effects include arteriolar vasoconstriction (increased resistance) and decreased excretion of salt and water by the kidneys (increased volume). These act to raise blood pressure.
 
Renin converts angiotensinogen into angiotensin I (AI). The angiotensin converting enzyme (ACE) then converts AI into angiotensin II (AII). AII is a potent vasoconstrictor, acting on arterioles both systemically and locally at the level of the kidney. AII also causes the release of ADH and aldosterone.
 
Aldosterone is secreted from the adrenal glands and acts to increase the reabsorption of salt from the Loop of Henle. Since water follows salt, this results in water retention as well. Aldosterone has a longer term impact on blood pressure control.
 
 
Anti-diuretic hormone (ADH), or vasopressin, is secreted from the posterior pituitary. It works on the kidney to increase the permeability of the collecting ducts, mediating its effect by inserting aquaporins into the ducts which helps increase the reabsorption of water.
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Summary

Blood pressure control is of central importance to physiologic balance, and there are numerous mechanisms at the local tissue level, within the central nervous system, and hormonally. These act in concert and at different speeds to respond to changes in blood pressure, maintaining healthy perfusion to vital and peripheral tissues.
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Resources and References

1) Guyton, A. C., Hall J. E. (2006). Textbook of Medical Physiology (11th ed.). Philadelphia, PA: Elsevier Saunders.
 
2) Andreoli T. E., Benjamin I. J., Griggs R. C., Wing E. J. (2010). Andreoli and Carpenter’s Cecil Essentials of Medicine (8th ed.). Philadelphia, PA: Elsevier Saunders.
 
3) Bickley L. S., Szilagyi P. G. (2009). Bates’ Guide to Physical Examination and History Taking (10th ed.). Philadelphia, PA: Wolters Kluwer Health - Lippincott Williams and Wilkins.

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