Hypertension, the chronic elevation of blood pressure, results in enhanced morbidity and mortality in the long run. However, researchers are not unanimous about the pathophysiology of hypertension. Studies over the years reveal that between 2 to 5 percent patients face elevated blood pressures because of underlying adrenal or renal disease. Rest of the patients, nonetheless, do not exhibit any clear and identifiable reason for the malady.
This statistics has well persuaded medical practitioners and researchers to acknowledge the role of multiple factors that might play varying roles in different patients of hypertension. Some of the most researched factors include salt intake, insulin resistance, obesity, and renin-angiotensin system. In recent years, though, some novel causes as genetics, neurovascular anomalies, endothelial dysfunction, and low birth weight have emerged as potential reasons of hypertension.
Further evidence reveals that the balance between cardiac output and peripheral vascular resistance is crucial to maintaining a normal blood pressure. Many patients with essential hypertension have been found to have a raised peripheral resistance. This pattern typically resembles primary hypertension due to various reasons including pheochromocytoma, renovascular disease, and aldosteronism. Some patients, however, have elevated cardiac output(CO) and inappropriately normal vascular resistance for the given level of CO. CO also increases because of disorders as thyrotoxicosis and aortic regurgitation. These anomalies also cause systolic hypertension.
The renin-angiotensin system is one of the most notable reasons to have affected the control of blood pressure. Renin, secreted from the kidney owing to the reduced salt intake, converts renin substrate to angiotensin I that is further converted rapidly into angiotensin II by the responsible enzyme. Angiotensin is known to increase blood pressure. It also releases aldosterone that results in a further increment of the blood pressure. Endothelin is a recently discovered vasoconstrictor that is likely to produce a salt sensitive rise in the blood pressure. It also modulates and activates the renin-angiotensin system. Endothelial dysfunction has also been implied by essential hypertension. It is because of the fact that vascular endothelial cells play a crucial role in cardiovascular regulation.
Of late, genetic factors have also fetched the attention of researchers who have been groping for some specific causes of high blood pressure. However, accuracy is lacking in the research, and it is still unknown what all specific genes are responsible for the rise. Nonetheless, statistics revealing that the children of hypersensitive parents are twice likely to suffer from the disease; it confirms the genetic aspect of hypertension. Some epidemiological studies have also suggested that genetic factors are responsible for around 30 percent variations in blood pressure across the members of different nationality and ethnic origin. Providing more insights to the findings, research studies have further suggested that kidney transplantation is one of the primary causes of inherited hypertension. For example, a kidney transplantation from a hypersensitive donor enhances the risk of the high blood pressure in the recipient. Last but not the least, while hypertension is rare in African tribes, it is quite common in Black populations of the US and the UK. This difference might be because of the lifestyle; researchers do confirm some genetic basis of this variation.
Reference
Gareth, G., Lip, G., & Brien, E. (2001, April 14). The Pathophysiology of Hypertension. ABC of Hypertension .
