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Essential Hypertension: Aetiology
Although essential hypertension by definition does not have any known cause, epidemiological studies have identified several risk factors for its development. All of these factors may not be identifiable in individual patients, underlying the heterogeneous nature of the essential hypertension population. Some of the important risk factors are discussed below.

I) Age:
Hypertension is predominantly a disorder of populations in which the fundamental problem is the tendency for blood pressure to rise with age. The14 systolic blood pressure rises till the 7th decade in males and sixth decade in females. Diastolic blood pressure rises till the 6th decade and then begins to fall.

II) Urban living:
Isolated2 communities in Africa and Asia do not show any age related increase in blood pressure. When they migrate to westernized societies, a rise in blood pressure is seen, indicating that environmental factors related to urban living are very important. Studies15 in India also show a lower prevalence of hypertension in the rural population, probably related to increased physical activity and low body mass index (BMI).

III) Social class:
Elevated16 blood pressure levels are seen more in the lower socio-economic strata. But it is difficult to predict its influence independent of other aspects of lifestyle related to hypertension, like alcohol, increased body- weight etc.

IV) Genetic factors:
Generic5 factors have long been assumed to be important in the genesis of hypertension. This is supported by familial aggregation studies, which show similar blood pressure values in first degree relatives. A17 positive family history is found in about 70% of the cases of essential hypertension. It13 is also estimated that children of hypertensive parents have a 45% chance of developing hypertension. However5 studies show a variation on the size of the genetic factor, again emphasizing the likely heterogeneous nature of the population with essential hypertension.

V) Dietary aspects:

A) BODY WEIGHT
There2 is definitive evidence that blood pressure is related to body weight, whether expressed as BMI, relative weight or skin fold thickness. Studies have also shown that blood pressure is more related to male pattern central obesity. Hypertension16 and obesity may also share common antecedents, both genetic and environmental. It may account for the clustering of hypertension, obesity, glucose intolerance and disorders of lipid metabolism, called Syndrome X. The role of insulin resistance, which is associated with obesity is also being examined as there are studies which show that it may have an effect independent of BMI

B) HIGH SALT INTAKE
There has been conflicting reports on the pathogenetic importance of salt intake. Evidence17 from epidemiological and migration studies show a positive association between salt intake and blood pressure. Treatment trials also show a reduction in blood pressure with salt reduction. However,5 there are some studies which show that only 60% of hypertensives are responsive to levels of sodium intake.

C) POTASSIUM
There16 is an inverse relationship between dietary potassium and blood pressure. Treatment trial also show a reduction in blood pressure levels with potassium supplementation.

D) CALCIUM
Several2 epidemiological studies have related a low calcium intake with high blood pressure levels. But calcium supplementation does not seem to have any effect on blood pressure.

E) ALCOHOL
There16 is a consistent positive association between alcohol consumption and blood pressure. This association is independent of other factors like age, BMI, social class etc. Intake14 of more than 6 units / day (I unit = ½ pint beer, one measure spirit, or I glass wine) increases the risk progressively.

F) NON VEGETARIAN DIET
Non1 vegetarians have a higher blood pressure at all ages compared to vegetarians. Cross over trials also have shown a lowering blood pressure with a change to a vegetarian diet

VI) Smoking:
Smoking16 causes an acute rise in blood pressure, but long term effects are unclear. While it may not have much of an effect on blood pressure itself, it has an important adverse effect on the prognosis of hypertensive cases

VII) Physical activity:
People16 with a sedentary lifestyle usually have higher blood pressure levels. Age related increase in blood pressure is seen less in the physically active and fit.. Many treatment trials also show that physical activity reduces arterial pressure, independent of changes in weight.

VIII) Stress:
Ambulstory4 blood pressure monitoring has shown a major rise in blood pressure levels during periods of acute pain, tension or mental stress. It has been suggested that some people may convert these normal transient hypertensive responses to stress into a sustained response. Consistent evidence to support this idea has always been difficult to find, because of the difficulty in measuring stress, and the wide individual variations in the response.
But it is becoming increasingly clear that psychological factors do have a role in initiating or maintaining hypertension. Essential18 hypertension is more prevalent in people who undergo mental stress during the course of their duties and those with "tense" personalities. Some16 of the studies have also implicated suppressed anger and lack of social support in the genesis of hypertension. Psychological stress may also be associated with other aspects of lifestyle linked with hypertension, like overeating, overdrinking, high calorie, high salt diet and physical inactivity.

IX) Intra uterine growth:
An16 inverse relationship between birth weight and adult blood pressure has received considerable attention. It is postulated that hypertension and other cardiovascular risk factors like obesity, NIDDM etc. may have common origin in poor development in utero or poor nutrition in infancy. The "syndrome X", thus may be more appropriately renamed as the "small baby syndrome".

X) Co-existing disease:
Hypertension16,18 and Diabetes Mellitus are often found together. In the hypertensive population, about 15 - 18% show some abnormality of glucose intolerance. As much as 50% of the diabetics may show elevated blood pressure levels. As noted earlier, hypertension, lipid abnormalities, obesity and glucose intolerance are seen clustered together.

Essential Hypertension : Pathogenesis

The exact pathogenetic mechanisms responsible for essential hypertension has been difficult to unravel, because of the variety of systems involved in the regulation of arterial pressure, and the complexity of their relationship with each other. Several abnormalities have been discovered in patients, with the claim that they are responsible for the rise in blood pressure. But there is accumulating evidence for the hypothesis that essential hypertension may have a number of distinct causes, operative in different subsets of the population.
It has also been observed that environmental factors held responsible do not operate on all the individuals. For example, the effect of stress or high salt intake is not seen on all the patients. It is possible that a genetic predisposition is needed, which determines the internal abnormalities through which the environmental factors operate. This inter-relationship between the environmental factors and a genetically determined failure of adaptation to these factors, may be the critical mechanism in the initiation of hypertension

The different abnormalities and pathogenetic mechanisms found in essential hypertension is discussed below.

1) Hyperactive sympathetic nervous system:
Stimulation19 of the sympathetic nervous system raises blood pressure, more in hypertensive or pre-hypertensive patients than in normotensives. This hyper responsiveness can often be detected before sustained hypertension develops, usually manifested as a high sleeping pulse rate. Even so, a higher than normal catecholamine levels are seen only in some patients. It is postulated that a genetically20 preconditioned over activity may be responsible for blood pressure elevation, in the face of environmental factors like stress, high salt intake etc.                  

2) The Renin-Angiotensin-Aldosterone mechanism:
Renin19, a proteolytic enzyme found in the juxta-glomerular apparatus cells, catalyses the conversion of the protein angiotensinogen to angiotensin I. This inactive product is cleaved by a converting enzyme into angiotensin II, which is a potent vasoconstrictor. It21 also stimulates the release of aldosterone from the suprarenal glands, which acts on the renal tubules causing salt and water retention, which further raises the blood pressure. The rennin-angiotensin system plays a very important part in maintaining a normal arterial pressure even in the presence of variation in other factors like salt intake. 

The role of renin in the pathogenesis of essential hypertension has been studied with interest. However, there5 is a broad range of plasma rennin activity in patients with essential hypertension and elevated levels are not found in the majority. It is usually normal in 60%, suppressed in 20% and elevated only in 15% of the cases.
It has been suggested instead of elevated renin levels, the primary abnormality may be an exaggerated aldosterone response to angiotensin II, at least in some patients. On a high sodium diet, blood pressure may be elevated in these patients because of the mild hyperaldosteronism.

3) Abnormal Sodium transport:
Abnormalities5 in sodium transport in red blood cells have been demonstrated in 35 - 50 % of the patients with essential hypertension. It is postulated that this abnormality may be present in vascular smooth muscle cells also. The resulting increase of intracellular sodium is followed by accumulation of calcium ions. Excess calcium in the cells increases the sensitivity of the vascular smooth muscle cells to presser stimuli, like sympathetic discharge.

4) Impaired pressure natriuresis:
Normally21 the blood pressure is maintained at a level that will allow adequate output of salt and water by the kidneys. This ensures that salt and water intake and output is equal over a long period. Whenever there is an excess of sodium and water in the body, blood pressure rises, causing the kidneys to excrete the salt and water. This is called pressure diuresis or pressure natriuresis.
It has been suggested13,17 that in some patients there may be a genetically determined defect in the kidney's ability to excrete excess sodium, except at high blood pressure levels. With the right environmental exposure (high sodium, low potassium diet ), the blood pressure may be increased as a compensatory mechanism to decrease sodium levels.

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