Elevated blood pressure (hypertension) affects both the function and the structure of blood vessels, largely small muscular arteries and arterioles. In this section, we discuss the mechanisms of normal blood preassure control, the possible mechanisms of hypertension, and the pathologic changes in the vasculature with the disorder.



A common health problem with widespread and some times devastating consequences, elevated blood pressure often remains asymptomatic until late in its course. Hypertension is one of the most important risk factors in both coronary heart disease and cerebrovascular accidents and may also lead to cardiac hypertrophy with heart failure ( hypertensive heart disease), arotic dissection, and renal failure. The detrimental effects of blood pressure increase continiously as the pressure rises. There is no rigidly defined threshold of blood pressure above which an individual is considered at risk for the complications of hypertension and below which an individual is safe. Neverthless a sustained diastolic pressure greater than 90 mm Hg or a sustained systolic pressure in excess of 140mm Hg is considered to consitute hypertension. By these criteria, screening programs reveal that 25% of persons in the general population are hypertensive. The prevalence increases with age. Black individuals are affected by hypertension about twice as often as whites and seem more vulnerable to is complications. Reduction of blood pressure has striking effects on incidence and death rates from ischemis heart disease, heart failure and stroke.

The major causes of hypertension about 90 to 95% of hypertension is idiopathic and apparently primary (essential hypertension). Of the remaining 5 to 10% most is secondary to renal disease or less often to narrowing of the renal artery, usually by an atheromatous plaque (renovascular hypertension). Infrequently, secondary hypertension is the result of disease related to the adrenal glands, such as primary aldosteronism. Cushing syndrome and phechromocytoma, or other disorders.

In most cases , hypertension remains at a modest level and fairly stable over years to decades and unless a myocardial infraction, heart failure, or cerebrovascular accident supervenes, is compatible with long life. About 5% of which, if untreated, leads to death within 1 or 2 years. This is called accelerated or malignant hypertension. The fullblown clinical syndrome of malignant hypertension includes severe hypertension (diastolic pressure > 120 mm Hg), renal failure, and retinal hemorrhages and exudates, with or without papilledema. This form of hypertension may develop in previously normotensive persons but more often is superimposed on preexisting hypertension, either essential or secondary. Visit for

The blood pressure level in any individual is a complex trait that is determined by the interaction of multiple genetic , environmental, and demographic factors. It should not be surprising therefore that multiple mechanisms play a role in hypertension. These mechanisms constitute aberrations of the normal psysiologic regulation of blood pressure.

Regulation of Normal Blood pressure.

The magnitude of the arterial pressure depends on two fundamental hemodynamic variables: cardiac output and total peripheral resistance. Cardiac output is influenced by blood volume, which is greatly dependent on body sodium. Thus sodium homeostasis is central to blood rpressure regulation. Total peripheral resistance is predominantly determined at the level of the arterioles and depends on lumen size itself dependent on the thickness of the arteriolar wall and the effects of neural and hormonal influences that either constrict or dilate these vessels. Normal vascular tone depends on the competition between vasoconstricting influences and vasodialators (including kinins, prostaglandins, and nitric oxide). Certain metabolic products (such as lactic acid, hydrogen ions, and adenosine) and hypoxia can also function as local vasodialators. Resistance vessels also exhibit autoregulation a process by which incerased blood flow to such vessels induces vasoconstriction an adaptive mechanism that protects against hyperfusion of tissues.

The kidneys play an important role in blood pressure and there is considerable evidence that renal dysfunction is essential for the development and maintenance of both essential and secondary hypertension.