Part of the TeachMe Series

Control of Blood Pressure

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Original Author(s): Abi Badrick
Last updated: 16th July 2023
Revisions: 26

Original Author(s): Abi Badrick
Last updated: 16th July 2023
Revisions: 26

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Blood pressure can be used to measure of how well our cardiovascular system is functioning. We all require a blood pressure high enough to supply organs with blood and nutrients they need, but not so high that blood vessels become damaged. Hence, control of blood pressure by different physiological mechanisms is essential. In this article, we will consider the mechanisms that control blood pressure, and some of the problems that can occur when control of blood pressure is lost.

Blood Pressure

The body’s blood pressure is a measure of the pressures within the cardiovascular system during the pumping cycle of the heart. It is influenced by a vast number of variables depending on the body’s demand. The blood pressure of each individual is slightly different and can change throughout the day depending on activity.

There is a range of normal blood pressures that are considered acceptable. The body tries to maintain a stable blood pressure through the process of homeostasis.

Blood pressure is measured using an automated blood pressure monitor, or manually using a stethoscope and sphygmomanometer. It is given as two values (e.g. 120/80 mmHg), measured in “millimetres of mercury (mmHg)”:

  • Systolic pressure – the first number (‘120 mmHg’ in the example) is the pressure of the blood during the heart contraction (systole).
  • Diastolic pressure – the second number (’80 mmHg’ in the example) is the pressure of the blood when the heart is at rest between heart beats (diastole).

Fig 1 – A sphygmomanometer and stethoscope being used to measure blood pressure.

Blood pressure can be calculated as:

Flow  x  Resistance


Mean arterial blood pressure  = Cardiac Output (flow)  x  Total Peripheral Resistance (resistance)


Therefore, these are factors that can affect blood pressure:

  • Cardiac output – the higher the cardiac output, the higher the volume of blood in the vessels. Therefore, this increases the pressure in the vessels.
  • Total peripheral resistance – a decrease in the diameter of the vessels, increases resistance and blood pressure.
  • Changes to blood viscosity and length of the blood vessels also alter resistance to blood flow.

Short-Term Regulation of Blood Pressure

Short-term regulation of blood pressure is controlled by the autonomic nervous system (ANS).

Changes in blood pressure are detected by baroreceptors. These are located in the arch of the aorta and the carotid sinus.

  • Increased arterial pressure stretches the wall of the blood vessel, triggering the baroreceptors. These baroreceptors then feedback to the autonomic nervous system. The ANS then acts to reduce the heart rate via efferent parasympathetic fibres (vagus nerve). This reduces the blood pressure.
  • Decreased arterial pressure is detected by baroreceptors, which trigger a sympathetic response. This stimulates an increase in heart rate and cardiac contractility leading to increased blood pressure.

Baroreceptors cannot regulate blood pressure long-term. This is because the mechanism that triggers baroreceptors resets itself once an appropriate blood pressure is reached.

Long-Term Regulation of Blood Pressure

There are several physiological mechanisms that regulate blood pressure in the long-term, such as the renin-angiotensin-aldosterone system (RAAS) and anti-diuretic hormone (ADH).

Renin-Angiotensin-Aldosterone System (RAAS)

Renin is a peptide hormone released by the granular cells of the juxtaglomerular apparatus in the kidney. It is released in response to:

  • Sympathetic stimulation
  • Reduced sodium-chloride delivery to the distal convoluted tubule
  • Decreased blood flow to the kidney

Renin facilitates the conversion of angiotensinogen to angiotensin I. This is then converted to angiotensin II using angiotensin-converting enzyme (ACE).

Angiotensin II is a potent vasoconstrictor. It acts directly on the kidney to increase sodium reabsorption in the proximal convoluted tubule. Sodium is reabsorbed via the sodium-hydrogen exchanger. Angiotensin II also promotes the release of aldosterone.

Aldosterone promotes salt and water retention by acting at the distal convoluted tubule to increase expression of epithelial sodium channels. Furthermore, aldosterone increases the activity of the basolateral sodium-potassium ATP-ase. This consequently, increases the electrochemical gradient for movement of sodium ions.

More sodium collects in the kidney tissue and water then follows by osmosis. This results in decreased water excretion and therefore increased blood volume and blood pressure.

ACE also breaks down a substance called bradykinin which is a potent vasodilator. Therefore, bradykinin breakdown increases the constricting effect. This potentiates the overall increase in blood pressure.

Fig 2 – A diagram outlining the RAAS and its actions on the body.

Anti-Diuretic Hormone (ADH)

The second mechanism by which blood pressure is regulated is via the Anti-Diuretic Hormone (ADH). It is produced in the hypothalamus and stored and released from the posterior pituitary gland. This is usually in response to thirst or an increased plasma osmolarity.

ADH acts to increase the permeability of the collecting duct to water by inserting aquaporin channels (AQP2) into the apical membrane.

It also stimulates sodium reabsorption from the thick ascending limb of the loop of Henle. This increases water reabsorption, thus increasing plasma volume and decreasing osmolarity.

Further Control of Blood Pressure

Other factors that can affect long-term regulation of blood pressure are natriuretic peptides. These include:

  • Atrial natriuretic peptide (ANP) is synthesised and stored in cardiac myocytes. It is released when the atria are stretched and indicates high blood pressure. ANP acts to promote sodium excretion by dilating the afferent arteriole of the glomerulus, increasing glomerular filtration rate (GFR). Moreover, ANP inhibits sodium reabsorption along the nephron. Conversely, ANP secretion is low when blood pressure is low.
  • Prostaglandins act as local vasodilators to increase GFR and reduce sodium reabsorption. Moreover, they act to prevent excessive vasoconstriction triggered by the RAAS and sympathetic nervous system.

Clinical Relevance – Hypertension

Hypertension is defined as a sustained increase in blood pressure above 140/90 mmHg. It may be primary (no known cause) or secondary to another condition such as chronic renal disease or Cushing’s syndrome.

Hypertension causes damage to the walls of blood vessels, making them weaker. This leads to macrovascular complications that affect larger vessels of the body (e.g. stroke or myocardial infarction). Additionally, it can result in microvascular complications affecting smaller vessels such as renal failure (nephropathy) or eye damage (retinopathy).

Hypertension also damages the heart itself by increasing the afterload of the heart. The heart must pump against greater resistance, leading to left ventricular hypertrophy or dilated cardiomyopathy. This may eventually lead to heart failure in the future. Hypertrophy of the cardiac muscle also increases the heart’s oxygen demand. As a result of this, myocardial ischaemia and ultimately angina may occur.

Hypertension is classified using the BHS thresholds for treatment:

Systolic BP (mmHg) Diastolic BP (mmHg)
Optimal <120 <80
Grade 1 (mild hypertension) 140-159 90-99
Grade 2 (moderate) 160-179 100-109
Grade 3 (severe) >180 >110


First-line pharmacological therapies may initially include ACE-inhibitors or calcium channel blockers. Lifestyle advice includes reducing salt intake and alcohol consumption, stopping smoking, and reducing intake of saturated fats.