The Pathophysiology of Hypertension
Published 02 Oct 2017
The article I chose bears the title “The Pathophysiology of Hypertension” and is authored by Gareth Beevers, Gregory Y.H. Lip and Eoin O’Brien. It was originally published in the British Medical Journal in April 14, 2001 and was made available in the online version of the journal.
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The authors acknowledge that there is no single factor to which hypertension, especially essential hypertension, can be attributed to. In the article, they reviewed all the known physiological mechanisms that work together to maintain blood pressure within a normal range. Then, they presented the possibilities in which failure of these mechanisms may contribute to hypertension.
There are many ways in which the body maintains normal blood pressure. First is through the balance between cardiac output (volume of blood pumped by the heart per minute) and peripheral vascular resistance (Beevers, Lip and O’Brien, 2001). Majority of hypertensive patients exhibit normal cardiac output but their arterioles register high resistance. This is because the smooth muscle cells associated with these vessels continuously contract. Hence, the blood vessels are also constantly constricted and begin to thicken, leading to permanent hypertension.
The renin-angiotensin-aldosterone (RAA) system also regulates blood pressure. Renin is released by the kidneys into the bloodstream where it acts upon the protein angiotensinogen. When converted to angiotensin II, it stimulates the adrenal gland to secrete aldosterone. The effect is that more sodium and water are retained in the body contributing to an increase in blood pressure. This, however, does not directly result in hypertension but localized renin in the heart, kidney and blood vessels may facilitate salt sensitive hypertension (Beevers, Lip and O’Brien, 2001).
The autonomic nervous system, in particular the symphathetic component, stimulates the kidneys to produce epinephrine and nor-epinephrine during periods of stress and intense physical activity (Beevers, Lip and O’Brien, 2001). These hormones increase constriction of the arterioles and subsequently, blood pressure. As with the RAA system, this has not been sufficiently proven to result in hypertension although it is established that blocking these hormones significantly lower blood pressure (Beevers, Lip and O’Brien, 2001).
A more significant contributory factor to hypertension is a defect in vascular endothelial cell functioning (Beevers, Lip and O’Brien, 2001). Endothelial cells produce nitric oxide, a vasodilator and endothelin, a vasoconstrictor and a stimulating factor of the RAA system. Malfunction may involve the inability of these cells to produce nitric oxide causing in a decreased capacity for vasodilation contributing to hypertension.
The atrial natriuretic hormone released by the right atrium of the heart is also an important regulator of blood pressure (Beevers, Lip and O’Brien, 2001). It acts to increase the rate in which the body loses water and sodium. This decreases blood volume, effectively lowering blood pressure. If the heart ceases to produce this hormone, the body loses a mechanism response to increases in blood pressure.
Hypertensive patients usually present with abnormal vessel walls, blood flow and composition which lead to hypercoagulability or blood clotting and increased blood pressure (Beevers, Lip and O’Brien, 2001). Evidence also suggests that genetics also contributes to the condition. Having one or both parents with hypertension increases the chances of their children developing the condition. Studies also reveal that genetic factors are responsible for 30% of the differences in blood pressure. It is also possible that the angiotensinogen gene and angiotensin converting enzyme are related to hypertension while the adducing gene may also contribute to salt sensitive hypertension (Beevers, Lip and O’Brien, 2001).
Hypertension in adolescence and adulthood has also been correlated with birth weight and certain congenital abnormalities (Beevers, Lip and O’Brien, 2001). Persons born with low birth weight have increased chances of developing hypertension than those born with normal birth weight. This is because low birth weight is also associated with metabolic abnormalities which are risk factors for hypertension (Beevers, Lip and O’Brien, 2001).
The clustering of multiple factors such as obesity, hypertension, glucose intolerance, diabetes mellitus and high blood cholesterol in patients who eventually suffer from ireversible hypertension and damage to the blood vessels suggest that all factors may in one way or another contribute towards the development of the condition (Beevers, Lip and O’Brien, 2001). The manner by which this occurs is still subject to research.
The article relates to physiology in that it describes how parts of the body, such as hormones, proteins and organs, normally function together to maintain the normal range of blood pressure. The disruption of normal functioning is shown to result in hypertension.
The article is comprehensive with respect to both known as well as contemplated factors related to the development of hypertension. However, recent updates regarding the progress of research in determining how each factor actually contributes to this condition have to be obtained. Prior knowledge regarding human anatomy is necessary to better appreciate the information presented. While there were tables, illustrations and graphs, these lacked visual appeal. Nevertheless, it served to deepen my cursory understanding of hypertension as a fairly common but not well understood illness. I recommend its reading to people with a background on anatomy and physiology or health-related subjects and who are interested primarily in contributory factors since the scope of the article did not include a definition of the condition, related diagnostic procedures, complications and management which relate to how normal physiological functioning can be restored in hypertensive patients.
List of References
- Beevers, G., Lip, G.Y.H. and O’Brien, E. (2001). “The Pathophysiology of Hypertension”. British Medical Journal 322(7291): 912-916. Retrieved 14 October 2008 from http://www.bmj.com/cgi/content/full/322/7291/912.