High blood pressure pathophysiology

High blood pressure Posted On


If you have a high blood pressure problem or you are curious to know about the blood pressure mechanism in-depth, then you are on the right site. 

In this article, you will get to know about the pathophysiology of high blood pressure.

Let’s firstly understand what blood pressure is?

Blood pressure means whatever pressure is produced by blood around the vessels is called blood pressure

Pressure may be high or low.

Increase blood pressure or hypertension is a common condition in which blood is consistently forced against the artery wall.

Hypertension is a leading cause to increase life-threatening complications like myocardial infarction, ischemic heart disease, renal failure, stroke, and other diseases.

Your blood pressure depends on the pumping organ – the heart. Blood is pumped from the heart to other parts of the body by vessels.

As per WHO (world health organization) report – around 1.13 billion people have hypertension worldwide.

Today we will understand the several physiological mechanisms that are responsible for hypertension.

High blood pressure


What does your blood pressure number mean?

Hypothetically normal blood pressure (BP) is 120/80 mmHg. But practically, it is difficult for you to get in this range. Your blood pressure fluctuates typically all over the day.

The upper number 120 is systolic blood pressure, whereas the lower number 80 is diastolic blood pressure.High blood pressure

Systolic BP is directly proportional to Cardiac output (CO), whereas Diastolic BP is directly proportional to Total peripheral resistance (TPR)

Systolic BP ∝ CO

Diastolic BP ∝ TPR


Therefore, systolic BP is dependent on CO, and diastolic BP is dependent on TPR.

It means if your CO increase, then systolic blood pressure will rise. Similarly, if TPR increases, then the diastolic pressure will also rise. 



What are systolic and diastolic blood pressures?

Systolic BP is the pressure present in the main artery when your heart muscles (left ventricle) are contracting (passing blood to the artery).

During this situation, your mitral valve (also called the bicuspid valve or left atrioventricular valve) is closed, and the aortic valve is open.

If there is more cardiac output, more chance of high systolic blood pressure.

As far as the concern of diastolic BP, those pressure occurs in the main artery while your heart muscle (left ventricle) is relaxing, called Diastolic BP. 

In that case, your mitral valve is open, and the aortic valve is closed.

If there is resistance in the peripheral artery, it will increase diastolic blood pressure.



How do biological factors affect your blood pressure?

As I mentioned above, systolic BP depends mainly on cardiac output (CO). But cardiac output also depends on several other factors.

Cardiac output (L/min) means the amount of blood ejected from ventricles in every minute. The average CO is approximately 5L/min.

Cardiac output can be calculated by this equation –

CO = Stroke volume (SV) x Heart rate (HR)


Heart rate means how many times your heart beats in every minute.

A normal heartbeat is 60 to 100 (72) beats/min.

Heart rate also affects Stroke volume. If your heart rate increases, you may have a high stroke volume. 


Stroke volume means the amount of blood ejected from ventricles with every beat. The average stroke volume is 70 ml.

Stroke volume is affected by three main factors – 


Preload – 

It depends on end-diastolic volume (EDV) 

EDV means the amount of blood present in the left ventricle just before contraction.

If your EDV is more, then stroke volume will be high.


Contractility – If the heart’s contractility (+ionotropic effect) is more, the stroke volume will be high. 


Afterload – 

It depends on end-systolic volume (ESV)

ESV means the volume of blood remaining in the ventricle after ejection.

If your ESV is less, then stroke volume will be high.

So, the equation comes after this – 

Stroke volume = EDV-ESV


Ok, now you suppose if you have a high blood volume.

It will increase venous return

Increase preload (increase EDV)

Increase stroke volume

Increase cardiac output

Increase systolic BP 


If your arterioles are collapse or resistance develops, then it will increase diastolic blood pressure.


What does the guideline say about blood pressure?

As per the American heart association –

Blood pressure category

Systolic and diastolic range (mmHg)


<120 and <80

Slightly elevated (Prehypertension)

120-129 and <80

Hypertension – stage 1

130-139 or 80-89

Hypertension – stage 2

≥140 or ≥90

Hypertensive crisis

>180 and/or >120




How does your blood pressure regulate by the autonomic nervous system?

Suppose you got an injury and you lost severe blood loss. Due to this, your blood pressure is low. 

Let’s see how your body regulates blood pressure in this circumstance.

If there is fluctuation in your blood pressure. Then your baroreceptor will be activated. 

Baroreceptors act as sensors that detect pressure change. It is present in your carotid sinus and aortic arch.

Carotid sinus and aortic arch send a signal to the nucleus of Tractus solitarius – central regulator (Medulla oblongata of brain stem) by afferent impulses.

The carotid sinus sends a signal via the 9th cranial nerve, which is called the glossopharyngeal nerve. In contrast, the aortic arch sends signals via the 10th cranial nerve called the vagus nerve.

Tractus solitarius regulates main three centers –

  1. Cardioinhibitory center (CIC) – arise parasympathetic nerve
  2. Cardioaccelerator center (CAC) – arise sympathetic nerve
  3. Vasomotor tone – arise sympathetic nerve

CIC When your blood pressure is low, tractus solitarius inhibits CIC, which decreases parasympathetic outflow or vagus outflow and decreases the release of acetylcholine (Ach).

CAC – CAC stimulates and increases sympathetic outflow to the heart, releasing norepinephrine (NE), which activates the SA node (Sinoatrial). This result causes increased heart rate, increased cardiac output, and ultimately hypertension problems.

Vasomotor tone – The vessel’s tone is modulated by the sympathetic system. It controls the veins, arteries, and adrenal medulla.

It stimulates the sympathetic nerve, which results on  –

High blood pressure


These biological factors may slightly increase blood pressure to maintain equilibrium or homeostasis.

In this way, the autonomic nervous system helps to regulate the short-term regulation of blood pressure.

Moreover, the kidney is also influenced by the sympathetic nerve, which helps to release renin. 


How does RAAS work?

RAAS is a long-term mechanism to regulate your blood pressure.

RAAS stands as the Renin Angiotensin Aldosterone System. It regulates blood pressure by handling blood volume, water, and sodium concentration.

Let’s understand by stepwise –

Step 1 – Stimulation of the sympathetic system

The kidney is a critical player in this system. We have seen above how the kidney is influenced by a sympathetic nerve.


Step 2 – Renin release

Generally, the Juxtaglomerular apparatus (JGA) has made up of three types of cells – polkissen cells, lacis cells, and macula densa (present in distal convoluted tubule). 

JGA is present in every glomerulus. 

Baroreceptor is also present in polkissen cells, which detect the pressure of renal perfusion.

Renin release in your systemic circulation by efferent arterioles based on response to one of three factors –

  • If JGA is stimulated by sympathetic nerve
  • If there is a decrease in renal perfusion that sense by the baroreceptor present in the afferent arteriole
  • If less sodium is detected by macula densa


Step 3 – Production of angiotensin

As you know, the liver has many vital functions; it helps produce a lot of proteins.

It releases angiotensinogen in your bloodstream. Angiotensinogen is an inactive protein that converts into angiotensin I (AT -I) by renin.

AT-I is a decapeptide that goes into the pulmonary circulation. Then AT-I is converted into Angiotensin II (AT-II) by angiotensin-converting enzyme (ACE).

ACE is present on endothelial cells of the lining of pulmonary vessels. Now, AT-II is a fully active protein.


Clinically, ACE inhibitor drugs are used to stop the conversion of AT-I to AT-II.


Step 4 – Binding of angiotensin II on receptor

AT-II binds on the angiotensin-II receptor (GPCR). It is present on –

I. Vessels – AT-II molecule binds on AT-II receptor then it increases calcium ions by the cellular mechanism. Eventually, it leads to vasoconstriction and arterial constriction.

Vasoconstriction – It causes increase blood volume, increase stroke volume, and increase cardiac output. As a result, increased systolic blood pressure.

Arterial constriction – It causes an increased total peripheral resistance (TPR), resulting in increased diastolic pressure.


II. Hypothalamus – AT-II binds to the hypothalamus and stimulates the central nervous system. Due to this, you feel thirsty. You may also feel a headache.


III. All sympathetic nerve ending – AT-II binds on this location, resulting in an excessive amount of norepinephrine release. Then it stimulates the heart and increases contractility. 


IV. Adrenal gland – It comprises three layers: zona glomerulosa, zona fasciculata, and zona reticularis. Zona glomerulosa is an outer layer where the AT-II receptor is present.

When AT-II binds to this receptor, it releases aldosterone from zona glomerulosa in general circulation.


Step – 5 Aldosterone secretion

Aldosterone is a mineralocorticoid – steroid hormone. It releases from zona glomerulosa, which causes fluid retention and electrolytes.

This means it increases sodium and water in your blood. 

Finally, it decreases sodium and water excretion in your urine. It increases the removal of more potassium from your body.

More retention of fluid causes hypertension. You may also feel more fatigue due to the loss of potassium.

Similarly, it reverses the all-action in hypertension by the autonomic nervous system and RAAS. It would be called a reverse feedback mechanism. 



We learned how our body tries to maintain blood pressure through different physiological mechanisms.

The mechanism of high blood pressure is very complex because many biological factors are involved in raising your blood pressure like –

  • Increased cardiac output (CO)
  • Increased Total peripheral resistance (TPR)
  • Increased cardiac contractility
  • Increased Heart rate (HR)
  • Increased Stroke Volume (SV)
  • Influences of sympathetic outflow
  • Vasoconstriction and arterial constriction
  • Influences of RAAS


Your current life is not easy. You face many situations like stress, unhealthy diet, lifestyles change, etc. Due to this, you get hypertension problems and other cardiac complications. 

The story is not finished yet. In my next blog, I will be explaining the causes of high blood pressure.

It is coming very soon.

I hope you enjoyed this article. 

If you found this post informative, please share it on social media. 


References – 


1. Physiology, Renin-Angiotensin System

2.  CDC

3. The cardio-inhibitory center

4. Cardiovascular physiology concepts


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