Etiology of essential hypertension
A number of environmental factors have been implicated in the development of hypertension, including salt intake, obesity, occupation, alcohol intake, family size, stimulant intake, excessive noise exposure, and crowding.
Sodium is the environmental factor that has received the greatest attention. It is to be noted that approximately 60% of the essential hypertension population is responsive to sodium intake.
Role of renin
Renin is an enzyme secreted by the juxtaglomerular cells of the kidney and linked with aldosterone in a negative feedback loop. The range of plasma renin activity observed in hypertensive subjects tends to be broader than in normotensive individuals. In consequence, some hypertensive patients have been defined as having low-renin and others as having high-renin essential hypertension. Low-renin hypertension is more common in African Americans than Caucasians and may explain why they tend to respond better to diuretic therapy than drugs that interfere with the renin-angiotensin system.
Insulin is a polypeptide hormone secreted by the pancreas. Its main purpose is to regulate the levels of glucose in the body. Insulin also exhibits vasodilatory properties. In normotensive individuals, insulin may stimulate sympathetic activity without elevating mean arterial pressure. However, in more extreme conditions such as that of the metabolic syndrome, the increased sympathetic neural activity may over-ride the vasodilatory effects of insulin. Insulin resistance and/or hyperinsulinemia have been suggested as being responsible for the increased arterial pressure in some patients with hypertension. This feature is now widely recognized as part of syndrome X, or the metabolic syndrome.
Sleep apnea is a common, under recognized cause of hypertension. It is best treated with weight loss, nocturnal nasal positive airway pressure, or the Mandibular advancement splint (MAS).
Hypertension is one of the most common complex genetic disorders, with genetic heritability averaging 30%. Data supporting this view emerge from animal studies as well as in population studies in humans. Most of these studies support the concept that the inheritance is probably multifactorial or that a number of different genetic defects each have an elevated blood pressure as one of their phenotypic expressions.
More than 50 genes have been examined in association studies with hypertension, and the number is constantly growing..
There are some anecdotal or transient causes of high blood pressure. These are not to be confused with the disease called hypertension in which there is an intrinsic physiopathological mechanism as described above.