Blood pressure and it's regulation



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Blood pressure and it's regulation


Blood pressure is measured using an automated blood pressure monitor, or manually using a 

stethoscope and sphygmomanometer. It is given as two values (eg 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.

 Diastolic pressure – the second number (80 mmHg in the example) is the pressure of 

the blood after one contraction but before the next contraction.

There are two basic mechanisms for regulating blood pressure: 

(1) Short-term mechanisms, which regulate blood vessel diameter, heart rate and contractility 

(2) Long-term mechanisms, which regulate blood volume

SHORT-TERM REGULATION OF BLOOD PRESSURE

Stimulation of baroreceptors in carotid sinus, aortic arch, and other large arteries of 

the neck and thorax 

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

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 and cardiac contractility via the 

efferent parasympathetic fibres (vagus nerve) thus reducing blood pressure.

 Decreased arterial pressure is detected by baroreceptors, which then trigger 

a sympathetic response.

 This stimulates an increase in heart rate and cardiac contractility leading to an increased blood pressure.


Baroreceptors cannot regulate blood pressure long-term. This is because the mechanism of 

triggering baroreceptors resets itself once a more adequate blood pressure is restored.

LONG-TERM REGULATION OF BLOOD PRESSURE

There are several physiological mechanisms that regulate blood pressure in the long-

term, the first of which is the renin-angiotensin-aldosterone system (RAAS).

Kidney Juxtaglomerular apparatus 

Juxtaglomerular cells: These cells are similar to epithelium and are located in the media of 

the afferent arterioles as they enter the glomeruli.

The juxtaglomerular cells secrete renin in response to:

 Decrease in renal perfusion pressure (detected directly by the granular cells)

 Decrease in NaCl concentration at the macula densa, often due to a decrease 

in glomerular filtration rate

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 which 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 release of aldosterone.

ACE also breaks down a substance called bradykinin which is a potent vasodilator. 

Therefore, the breakdown of bradykinin potentiates the overall constricting effect.

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, thus increasing 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 thus blood pressure.

Anti-Diuretic Hormone (ADH)

The second mechanism by which blood pressure is regulated is release of Anti Diuretic 

Hormone (ADH) from the OVLT of the hypothalamus 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, indicating of high blood pressure.

 ANP acts to promote sodium excretion. It dilates the afferent arteriole of the 

glomerulus, increasing blood flow (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. They also act to prevent excessive vasoconstriction triggered by the 

sympathetic nervous and renin-angiotensin-aldosterone systems.

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