Hypertension, or high blood pressure, occurs in about 25% of the population and is defined by a sustained dias-tolic pressure greater than 90 mmHg or a sustained systolic pressure greater than 140 mmHg. Hypertension is often as-sociated with atherosclerotic vascular disease and with an increased risk of cardiovascular disorders such as stroke and angina pectoris. In most cases of hypertension, the luminal diameter of small muscular arteries and arterioles is reduced, which leads to increased vascular resistance. Re-striction in the luminal size may also result from active con-traction of smooth muscle in the vessel wall, an increase in the amount of smooth muscle in the wall, or both. In individuals with hypertension, smooth muscle cells multiply. The additional smooth muscle then adds to the thickness of the tunica media. Concomitantly, some of the smooth muscle cells accumulate lipid. This is one reason why hypertension is a major risk factor for atherosclerosis. In fat-fed animals, hypertension accelerates the rate of lipid accumulation in vessel walls. In the absence of a fatty diet, hypertension increases the rate of intimal thickening that occurs naturally with age. Cardiac muscle is also affected by chronic hypertension that leads to pressure overload, resulting in compensatory left ventricular hypertrophy. Ventricular hypertrophy in this condition is caused by an increased diameter (not length) of cardiac muscle cells with characteristic enlarged and rectangular nuclei. Left ventricular hypertrophy is a com-mon manifestation of the hypertensive heart disease. Ventricular hypertrophy makes the wall of the left ventricle uniformly much thicker and less elastic, and the heart must then work harder to pump blood (Fig. F13.2.1). Untreated hypertensive heart disease would lead to cardiac failure. Recent studies have shown that prolonged reduction of blood pressure in patients with ventricular hypertrophy as a result of chronic hypertension can reduce the degree of hypertrophy. normal wall of right ventricle hypertrophied wall of left ventricle FIGURE F13.2.1 • Horizontal section of the heart with left ventricular hypertrophy. This photograph shows a cross section of the ventricles of the heart from a patient with chronic hypertension. The walls of the left ventricle are concentrically thickened, resulting in decreases of the cavity diameter. Note the wall of the right ventricle, which has normal dimensions. (Reprinted with permission from Rubin R, Strayer DS. Rubin’s Pathology. 5th ed. Baltimore: Lippincott Williams & Wilkins, 2008.)  The subendothelial layer of connective tissue in larger elastic arteries consists of connective tissue with both collagen and elastic fibers. The main cell type in this layer is the smooth muscle cell. It is contractile and secretes extracellular ground substance as well as collagen and elastic fibers. Occasional macrophages may also be present.
 The internal elastic membrane in elastic arteries is not conspicuous because it is one of many elastic layers in the wall of the vessel. It is usually identified only because it is the innermost elastic layer of the arterial wall.
Endothelial cells participate in the structural and functional integrity of the vascular wall.
Endothelial cells not only provide a physical barrier between the circulating blood and the subendothelial tissues but also produce vasoactive agents that cause constriction and relaxation of underlying vascular smooth muscles.
Multiple roles and functions of the endothelium lining of blood vessels are described in detail at the beginning of this chapter (see page 409).
The tunica media of elastic arteries consists of multiple layers of smooth muscle cells separated by elastic lamellae.
The tunica media is the thickest of the three layers of elastic arteries and consists of the following.