Essential Hypertension

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The vast majority of people with hypertension have essential hypertension. An increased total peripheral resistance is a universal characteristic of this condition. Cardiac rate and the cardiac output are elevated in many, but not all, of these cases.

The secretion of renin, which is correlated with an-giotensin II production and aldosterone secretion, is likewise variable. Although some people with essential hypertension have low renin secretion, most have either normal or elevated levels of renin secretion. Renin secretion in the normal range is inappropriate for people with hypertension, since high blood pressure should inhibit renin secretion and, through a lowering of aldosterone, result in greater excretion of salt and water. Inappropriately high levels of renin secretion could thus contribute to hypertension by promoting (via stimulation of aldosterone secretion) salt and water retention and high blood volume.

Sustained high stress (acting via the sympathetic nervous system) and high salt intake appear to act synergistically in the development of hypertension. There is some evidence that Na+ enhances the vascular response to sympathetic stimulation. Further, sympathetic nerve stimulation can cause constriction of the renal blood vessels and thus decrease the excretion of salt and water.

As an adaptive response to prolonged high blood pressure, the arterial wall becomes thickened. This response can lead to arteriosclerosis and results in an even greater increase in total peripheral resistance, thus raising blood pressure still more in a positive feedback fashion.

The interactions between salt intake, sympathetic nerve activity, cardiovascular responses to sympathetic nerve activity, kidney function, and genetics make it difficult to sort out the cause-and-effect sequence that leads to essential hypertension. Current evidence suggests that the inability of the kidneys to properly eliminate salt and water is a shared characteristic in all cases of essential hypertension. Further, there is evidence that salt intake may be the single most important factor. Chimpanzees with their natural, low-salt diet, have low blood pressure. When given human levels of dietary salt, however, their blood pressure rises. "Pre-literate" people whose diet is natural and low in salt similarly exhibit low blood pressure that does not

Cardiac Output, Blood Flow, and Blood Pressure


Table 14.10 Mechanisms of Action of Selected Antihypertensive Drugs

Category of Drugs Examples Mechanisms


Sympathoadrenal system inhibitors

Thiazide; furosemide Clonidine; alpha-methyldopa

Guanethidine; reserpine Atenolol


Increase volume of urine excreted, thus lowering blood volume

Act to decrease sympathoadrenal stimulation by bonding to (^-adrenergic receptors in the brain Deplete norepinephrine from sympathetic nerve endings Blocks beta-adrenergic receptors, decreasing cardiac output and/or renin secretion

Blocks alpha-adrenergic receptors, decreasing sympathetic vasoconstriction

Direct vasodilators

Hydralazine; minoxidil sodium nitroprusside

Cause vasodilation by acting directly on vascular smooth muscle

Calcium channel blockers

Angiotensin-converting enzyme (ACE) inhibitors Angiotensin II-receptor antagonists

Verapamil; diltiazem Captopril; enalapril Losartan

Inhibit diffusion of Ca2+ into vascular smooth muscle cells, causing vasodilation and reduced peripheral resistance Inhibit the conversion of angiotensin I into angiotensin II

Blocks the binding of angiotensin II to its receptor

rise with age. Even though some people may be more salt-sensitive than others, these findings suggest that everyone with hypertension should restrict their intake of dietary salt.

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