Pathophysiology of Hypertension

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A variety of systems are involved in the regulation of Blood Pressure (BP): renal, hormonal, vascular, peripheral and central adrenergic systems. BP is the product of Cardiac Output (CO) and Total Peripheral Resistance (TPR): BP = CO × TPR[1] . The pathogenic mechanisms leading to hypertension must lead to increased TPR by inducing vasoconstriction, to increased CO, or to both. Hypertension is frequently associated with a normal CO and elevated TPR[2] .

The pathophysiology of hypertension is not well understood. In more than 95% of cases, the etiology of hypertension is unknown and is called primary, essential or idiopathic hypertension, whereas secondary hypertension refers to a known etiology[3] .


Essential hypertension tends to cluster in families and represents a collection of genetically based diseases and syndromes with a number of underlying inherited biochemical abnormalities[4] . Factors considered important in the genesis of essential hypertension include[5] :

· Genetic. Hypertension runs in families. Children of hypertensive parents are twice as likely to develop hypertension as are children of normotensive parents.
· Dietary. Dietary factors that contribute to hypertension include high sodium, saturated fat and cholesterol intake.
· Obesity. Usually linked with both a poor diet and physical inactivity.
· Age. Clinical signs of hypertension usually appear after age 40.
· Race. More black than white people are clinically diagnosed with hypertension each year.
· Stress. During stress, the sympathetic nervous system is mobilised causing blood vessels to constrict and heart rate to increase. Together these factors raise blood pressure.
· Smoking. Nicotine enhances the sympathetic nervous systems vasoconstrictor effects.
· Renin Secretion. Inappropriate renin secretion by the kidneys results in an increase in both vasoconstriction and mean arterial BP.

Essential hypertension cannot be cured, but most cases can be controlled by consuming a balanced diet with limited salt, fat and cholesterol intake, engaging in regular exercise, stopping smoking, managing stress and taking antihypertensive drugs[6] .












YouTube Video: Hypertension[7]


Although secondary hypertension forms a small percentage of hypertension cases, recognising these cases is important because they can often be improved by surgery or specific medical therapy. The majority of secondary forms of hypertension are renal or endocrine hypertension. Renal hypertension is usually attributed to a derangement in the renal handling of sodium and fluids, leading to volume expansion or an alteration in renal secretion of vasoactive materials resulting in a systemic or local change in arterial tone[8] . Endocrine hypertension is usually attributed to an abnormality of the adrenal glands[9] .
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Prolonged hypertension is the major cause of heart failure, vascular disease, renal failure and stroke. When the heart is forced to pump against greater resistance, it must work harder, and in time the myocardium enlarges. When finally strained beyond its capacity to respond, the heart weakens and blood vessels become damaged, causing small tears in the endothelium that accelerates the progress of atherosclerosis[10] . As the vessels become increasingly blocked, blood flow to the tissues becomes inadequate and vascular complications appear in the brain, heart, kidneys and retinas of the eyes[11] .

Blood flow through body tissues is involved in delivery of oxygen and nutrients, removal of waste, gas exchange in lungs, absorption of nutrients from the digestive tract and urine formation in the kidneys[12] . The hearts’ demand for oxygen is increased with hypertension and thus renders the heart more susceptible to angina or myocardial infarction.


Atherosclerosisis characterised by an accumulation of lipids, inflammatory cells and connective tissue within the arterial intimal layer[13] . High blood pressure forces blood to move through arteries and arterioles at high pressure which damages the vessels. White blood cells are then drawn to the damaged area to form atherosclerotic plaque.

The blood vessels of the Brain can also be damaged and result in a build-up of atherosclerotic plaque. Further, high BP can cause clots to break off from the atherosclerotic plaque and block blood flow to the rest of the brain, resulting in a thrombotic stroke[14] . Continual exposure to high BP can also cause a blood vessel of the brain to burst, leading to a hemorrhagic stroke.

Kidney damage occurs when high blood pressure causes the capillaries to breakdown and become permeable to proteins and other molecules[15] . This causes the kidneys tubules to become clogged and decrease the ability to make urine.

Finally the Retinas of the eye can be damaged if their delicate capillaries are damaged by prolonged high BP. This damage can cause localised haemorrhaging and the formation of scar tissue and new imperfect capillaries[16] .

Read more: http://www.givehowto.com/high-blood-pressure-signs-and-symptoms-do-not-ignore-them-and-put-you-at-risk/


external image Atherosclerosis.jpg






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  1. ^



    Contractor, A. & Gordon, N. Cited from: Ehrman, J. K., Gordon, P. M., Visich, P. S., & Keteyian, S. J. (2009). Clinical Exercise Physiology. Human Kinetics.
  2. ^ Contractor, A. & Gordon, N. Cited from: Ehrman, J. K., Gordon, P. M., Visich, P. S., & Keteyian, S. J. (2009). Clinical Exercise Physiology. Human Kinetics.
  3. ^



    Durstine, L. J., Moore, G. E., Painter, P. L., & Roberts, S. O. (2009). ACSM'S Exercise Management for Persons with Chronic Diseases and Disabilities. American College of Sports Medicine.
  4. ^



    Contractor, A. & Gordon, N. Cited from: Ehrman, J. K., Gordon, P. M., Visich, P. S., & Keteyian, S. J. (2009). Clinical Exercise Physiology. Human Kinetics.
  5. ^



    Marieb, E. N. (2004). Human Anatomy & Physiology. San Francisco: Pearson Education, Inc.
  6. ^



    Marieb, E. N. (2004). Human Anatomy & Physiology. San Francisco: Pearson Education, Inc.
  7. ^



    Cited From YouTube: Hypertension. http://www.youtube.com/watch?v=xnyfElxkBlI&feature=related
    On 28/03/2011
  8. ^



    Contractor, A. & Gordon, N. Cited from: Ehrman, J. K., Gordon, P. M., Visich, P. S., & Keteyian, S. J. (2009). Clinical Exercise Physiology. Human Kinetics.
  9. ^ Contractor, A. & Gordon, N. Cited from: Ehrman, J. K., Gordon, P. M., Visich, P. S., & Keteyian, S. J. (2009). Clinical Exercise Physiology. Human Kinetics.
  10. ^



    Marieb, E. N. (2004). Human Anatomy & Physiology. San Francisco: Pearson Education, Inc.
  11. ^ Marieb, E. N. (2004). Human Anatomy & Physiology. San Francisco: Pearson Education, Inc.
  12. ^



    Marieb, E. N. (2004). Human Anatomy & Physiology. San Francisco: Pearson Education, Inc.
  13. ^



    Contractor, A. & Gordon, N. Cited from: Ehrman, J. K., Gordon, P. M., Visich, P. S., & Keteyian, S. J. (2009). Clinical Exercise Physiology. Human Kinetics.
  14. ^



    Marieb, E. N. (2004). Human Anatomy & Physiology. San Francisco: Pearson Education, Inc.
  15. ^



    Marieb, E. N. (2004). Human Anatomy & Physiology. San Francisco: Pearson Education, Inc.
  16. ^



    Marieb, E. N. (2004). Human Anatomy & Physiology. San Francisco: Pearson Education, Inc.