Figure 1914

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Analysis of arterial pressure regulation in (1) nonsalt-sensitive essential hypertension and (2) salt-sensitive essential hypertension. (Redrawn from Guyton AC, Coleman TG, Young DB, et al: Salt balance and long-term blood pressure control. Annu Rev Med 31:15, 1980. With permission, from the Annual Review of Medicine, © 1980, by Annual Reviews http://www.AnnualReviews.org.)

increasing the level of sodium intake. The sodium-loading type of curve can be determined by increasing the level of sodium intake to a new level every few days, then waiting for the renal output of sodium to come into balance with the intake, and at the same time recording the changes in arterial pressure.

When this procedure is used in essential hypertensive patients, two types of curves, shown to the right in Figure 19-14, can be recorded in essential hypertensive patients, one called (1) nonsalt-sensitive hypertension and the other (2) salt-sensitive hypertension. Note in both instances that the curves are shifted to the right, to a much higher pressure level than for normal people. Now, let us plot on this same graph (1) a normal level of salt intake and (2) a high level of salt intake representing 3.5 times the normal intake. In the case of the person with nonsalt-sensitive essential hypertension, the arterial pressure does not increase significantly when changing from normal salt intake to high salt intake. Conversely, in those patients who have salt-sensitive essential hypertension, the high salt intake significantly exacerbates the hypertension.

Two additional points should be emphasized: (1) Salt-sensitivity of blood pressure is not an all-or-none characteristic—it is a quantitative characteristic, with some individuals being more salt-sensitive than others. (2) Salt-sensitivity of blood pressure is not a fixed characteristic; instead, blood pressure usually becomes more salt-sensitive as a person ages, especially after 50 or 60 years of age.

The reason for the difference between nonsalt-sensitive essential hypertension and salt-sensitive hypertension is presumably related to structural or functional differences in the kidneys of these two types of hypertensive patients. For example, salt-sensitive hypertension may occur with different types of chronic renal disease due to gradual loss of the functional units of the kidneys (the nephrons) or to normal aging as discussed in Chapter 31. Abnormal function of the renin-angiotensin system can also cause blood pressure to become salt-sensitive, as discussed previously in this chapter.

Treatment of Essential Hypertension. Current guidelines for treating hypertension recommend, as a first step, lifestyle modifications that are aimed at increasing physical activity and weight loss in most patients. Unfortunately, many patients are unable to lose weight, and pharmacological treatment with antihy-pertensive drugs must be initiated.

Two general classes of drugs are used to treat hypertension: (1) vasodilator drugs that increase renal blood flow and (2) natriuretic or diuretic drugs that decrease tubular reabsorption of salt and water.

Vasodilator drugs usually cause vasodilation in many other tissues of the body as well as in the kidneys. Different ones act in one of the following ways: (1) by inhibiting sympathetic nervous signals to the kidneys or by blocking the action of the sympathetic transmitter substance on the renal vasculature, (2) by directly relaxing the smooth muscle of the renal vasculature, or (3) by blocking the action of the

—— Renin-angiotensin-vasoconstriction

—— Renin-angiotensin-vasoconstriction

Seconds Minutes Hours Days

Time after sudden change in pressure

Seconds Minutes Hours Days

Time after sudden change in pressure

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