What are the risk factors associated with hypertension

Patients with arterial hypertension and no definable cause are said to have primary, essential, or idiopathic hypertension.

Undoubtedly, the primary difficulty in uncovering the mechanism(s) responsible for the hypertension in these patients is attributable to the variety of systems that are involved in the regulation of arterial pressure-peripheral and / or central adrenergic, renal, hormonal and vascular-and to the complexity of the relationships of these systems to one another.

Several abnormalities have been described in patients with essential hypertension, often with a claim that one or more of these are primarily responsible for the hypertension.

While it is still uncertain whether these individual abnormalities are primary or secondary, varying expressions of a single disease process or reflective of separate disease entities, the accumulating data increasingly support the latter hypothesis.

Therefore, just as pneumonia is caused by a variety of infectious agents, even though the clinical picture observed may be similar, so essential hypertension likely has a number of distinct causes.

Thus the distinction between primary and secondary hypertension has become blurred, and the approach to both the diagnosis and therapy of hypertensive patients has been modified.

For example, as a group of patients with essential hypertension is separated into a distinct suset(eg., low-renin essential hypertension), such patients have not been reclassified as having a form of secondary hypertension but rather remain in the essential hypertensive group.

Those individuals with a specific structural organ defect responsible for hypertension are defined as having a secondary form of hypertension. In contrast, individuals who may have generalized functional abnormalities causing their hypertension, even if discrete are defined as having essential hypertension.

Heridity:

Genetic factors have long been assumed to be important in the genesis of hypertension. Data supporting this view can be found in animal studies as well as in population studies in humans.

One approach has been to assess the correlation of blood pressure within families. From these studies the minimum size of the genetic factor can be expressed by a correlation coefficient of approximately 0.2.

However, the variation in the size of the genetic factor in different studies reemphasizes the likely heterogeneous nature of the essential hypertensive population.

Additionally, most studies support the concept that the inheritance is probably multi-factorial or that a number of different genetic defects each have as one of their phenotypic expressions an elevated blood pressure.

Finally, monogenic defects have now been reported which have as one of their consequences an increased arterial pressure, e.g glucocorticoid-remedial aldostrenism.

Environment: A number of environmental factors have been specifically implicated in the development of hypertension, including salt intake, obesity, occupation, alcohol intake, family size and crowding.

These factors have all been assumed to be important in the increase in blood pressure with age in more affluent societies, in contrast to the decline in blood pressure with age in more primitive cultures.

Salt Sensitivity:

The environmental factor which has received the greatest attention is salt intake. Even this factor illustrates the heterogenous nature of the essential hypertensive population in that the blood pressure in only approximately 60 percent of hypertensives is particularly responsive to the level of sodium intake.

The cause of this special sensitivity to salt varies, with primary aldosteronism, bilateral renal artery stenosis, renal parenchymal disease, or low rennin essential hypertension accounting for about half the patients.

In the remainder, the pathophysiology is still uncertain, but recent postulated contributing factors include chloride, calcium a generalized cellular membrane defect, insulin resistance and nonmodulation.

Role of rennin: Renin is an enzyme secreted by the juxtaglomerular cell of the kidney and linked with aldosterone in a negative feedback loop.

While a variety of factors can modify this secretion, the primary determinant is the volume status of the individual, particularly as related to changes in dietary sodium intake.

The end product of the action of rennin on its substrate is the generation of the peptide angiotension II. The response of target tissues to this peptide is uniquely determined by the prior dietary electrolyte intake.

For example, sodicum intake normally modulates adrenal and renal vascular responses to angiotensin II. With sodium restriction, adrenal responses are enhanced and the renal vascular responses reduced.
Sodium loading has the opposite effect.

The range of plasma rennin activities observed in hypertensive subjects is more broad than in normotensive individuals. Thus some hypertensive patients have been defined as having low-renin and others as having high rennin essential hypertension.

| Clinical assessments and investigations involved in Hypertension | Hypertension - Clinical presentation of target organs | Causes of Secondary Hypertension | Treating Hypertension Clinically |

 

Main Menu

Add to My Yahoo!

FREE Subscription

Signup for Our Newsletter and Receive up to Date Details on Important Issues Affecting your Health.

Name:

Email:

Note : We never rent, trade, or sell our email lists to anyone. We assure that your privacy is respected and protected.

 

 

 





Disclaimer : All the material contained on this page is been just provided for educational and informational purposes only and not intended to any type of consultation. Please consult with your physician or appropriate healthcare personal for any kind of opinions or recommendations with respect to your symptoms or medical condition. The author is not responsible to any person or entity with respect to any kind of damage, loss, or injuries, caused or alleged to be caused directly or indirectly by the information contained in this report. Also, the logos, trademarks, and brand names, if any, depicted on this site are exclusive property of their respective companies.

Copyright - © 2004 - 2017 - All Rights Reserved.

|Privacy Policy | Disclosure | Contact |