Classification Of Systemic Hypertension: Essential And Secondary Hypertension

According to WHO in 1978, when blood pressure is elevated without an evident organic cause, it is called essential hypertension. Hypertension produced by an identifiable cause is called secondary hypertension.

Causes of secondary hypertension

1. Vascular causes: Coarctation of aorta, polyarteritis nodosa.
2. Renal causes: Renal artery stenosis, glomerulonephritis, pyelonephritis, radiation nephritis, nephrocalcinosis, tuberculosis of the kidney, polycystic disease of kidneys and renal tumours (hypernephroma).
3. Endocrine causes: Diseases of adrenal cortex, primary hyperaldosteronisms and cushing’s syndrome. Diseases of adrenal medulla: Pheochromocytoma.
4. Adverse reaction to drugs: e.g, Oral contraceptives, liquorice and carbenoxolone, corticosteroids and ACTH, sympathomimetic amines, tricyclic antidepressants when taken along with cheese, etc.
5. Toxemias of pregnancy.

In several surveys conducted in India, the prevalence has been found to vary between 10 and 15%. Essential hypertension forms 95-98% of the total and secondary hypertension forms only 1 to 2%. The age group between 40 and 60 years is affected most. Both sexes are affected equally. The following factors contribute to the occurrence of this condition:

1. Genetic factors: Essential hypertension shows a polygenic pattern of inheritance.
2. Psychological stress: Persons who have to undergo mental stress during the course of their duties and those with tense personality are affected more.
3. Salt and water intake: Communities with high salt intake have a higher prevalence of essential hypertension.
4. The renal hormones: The role of rennin-angiotensin-aldosterone system has been extensively studies. Renin is produced by the juxtaglomerular apparatus in response to various stimuli. The control of rennin release is complex. Several stimuli lead to rennin release. These are:

• The impulses from pressor receptors in the afferent arterioles of the glomeruli
• Chemo-receptors of the macula densa which are stimulated by hyponatremia
• The sympathetic stimuli which lead to rennin release on assuming the upright posture; and
• Chemical stimuli such as hypokalemia, etc. Rennin converts angiotensinogen to angiotensin I, which is further converted to angiotensin II, by the converting enzyme. Angiotensin II stimulates the production of aldosterone. Angiotensin II causes vasoconstriction and aldosterone leads to retention of salt and water. Among the hypertensive, 60% have normal, 30% have low and 10% have high values of plasma rennin activity.

Other factors such as deficiency of prostaglandins and kinnins which normally help in lowering the vascular tone have also be incriminated in the production of essential hypertension.