Hypertension is defined as a chronically increased systemic arterial pressure. The dividing line between normal pressure and hypertension is set at approximately 140/90 mmHg.
Theoretically, hypertension could result from an increase in cardiac output or in total peripheral resistance, or both. In reality, however, the major abnormality in most cases of well-established hypertension is increased total peripheral resistance caused by abnormally reduced arteriolar radius.
What causes the arteriolar constriction? In only a small fraction of cases is the cause known. For example, diseases that damage a kidney or decrease its blood supply are often associated with renal hypertension. The cause of the hypertension is increased release of renin from the kidneys, with subsequent increased generation of the potent vasoconstrictor angiotensin II. However, for more than 95 percent of the individuals with hypertension, the cause of the arteriolar constriction is unknown. Hypertension of unknown cause is called primary hypertension (formerly "essential hypertension").
Many hypotheses have been proposed to explain the increased arteriolar constriction of primary hypertension. At present, much evidence suggests that excessive sodium retention is a contributing factor in genetically predisposed ("salt-sensitive") persons. Many persons with hypertension show a drop in blood pressure after being on low-sodium diets or receiving drugs, termed diuretics, that cause increased sodium loss via the urine. Low dietary intake of calcium has also been implicated as a possible contributor to primary hypertension. Obesity and a sedentary lifestyle are definite risk factors for primary hypertension, and weight reduction and exercise are frequently effective in causing some reduction of blood pressure in persons with hypertension. Cigarette smoking, too, is a definite risk factor.
Hypertension causes a variety of problems. One of the organs most affected is the heart. Because the left ventricle in a hypertensive person must chronically pump against an increased arterial pressure (after-load), it develops an adaptive increase in muscle mass (left ventricular hypertrophy). In the early phases of the disease, this helps maintain the heart's function as a pump. With time, however, changes in the organization and properties of myocardial cells occur, and these result in diminished contractile function and heart failure (see below). The presence of hypertension also enhances the development of atherosclerosis and heart attacks (see below), kidney damage, and rupture of a cerebral blood vessel, which causes localized brain damage—a stroke.
The major categories of drugs used to treat hypertension are summarized in Table 14-11. These drugs all act in ways that reduce cardiac output and/or total peripheral resistance. You will note in subsequent sections of this chapter that these same drugs are also used in the treatment of heart failure and in both the prevention and treatment of heart attacks. One reason for this overlap is that these three diseases are causally interrelated; for example, as noted in this section, hypertension is a major risk factor for the development of heart failure and heart attacks. But in addition, the drugs often have multiple cardiovascular effects, which may play different roles in the treatment of the different diseases.
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