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Systemic blood pressure is related to vascular smooth muscle tone. At the cellular level, postsynaptic a and a2 receptors are stimulated by norepinephrine released from the presynaptic sympathetic nerve ending, ultimately leading to the release of intracellular calcium stores. Calcium release results in smooth muscle contraction via activation of actin and myosin. The increase in smooth muscle tone results in increased peripheral vascular resistance thereby causing increased blood pressure. The presynaptic a2 receptors, when stimulated by norepinephrine, help to limit this response by preventing further release of norepinephrine through a negative-feedback loop.

There are two major theories to explain how hypertension develops: (1) as a result of alterations in the contractile properties of smooth muscle in arterial walls, or (2) as a response to failure of normal autoregulatory mechanisms. Most individuals with hypertension have elevated peripheral vascular resistance with normal cardiac output. However, some patients may also have elevated cardiac output as a result of increased a-adrenergic and b-adrenergic tone.

The concept of autoregulation is important in the vascular beds of the vital organs, including the heart, kidneys, and brain, but has been most extensively studied in the latter.6 In the brain, as blood pressure falls, cerebral vasodilation occurs. When blood pressure rises, the autoregulatory response is vasoconstriction, ensuring a stable cerebral blood flow rate among a range of blood pressures. However, autoregulation is effective only within a specific range of blood pressures. Most authorities specify a range of 50 to 150 mmHg for MAP, within which there is effective autoregulation in an uninjured brain. At pressures beyond this narrow range, the limits of autoregulation are breached, and hypoperfusion or hyperperfusion results. In patients with chronically elevated blood pressure, the narrow range at which autoregulation functions is shifted higher. Thus, chronically hypertensive patients can develop symptoms of brain hypoperfusion if their blood pressure is lowered to "normal" levels, because normal levels may be below the limits of the individual's adjusted autoregulation. The lower limit of cerebral autoregulation is based on a patient's baseline MAP and is generally about 25 percent below this baseline. 6

When poorly controlled blood pressure is allowed to persist long enough, it can cause damage to specific organs and vascular beds. The pathologic change responsible for target-organ damage is fibrinoid necrosis of small arterioles. At a microscopic level, this process begins when vessels in capillary beds dilate in response to an elevated blood pressure that overwhelms the autoregulatory mechanism. The persistently elevated pressures cause injury to the endothelium, leading to increased vascular permeability and vascular wall injury. Eventually, endothelial damage leads to deposition of fibrin within the vessel walls and causes activation of mediators of coagulation and cell proliferation.Z A recurrent cycle of vascular reactivity develops, with an increased release of vasoconstrictors, endothelial damage, platelet aggregration, myointimal proliferation, and progressive narrowing of arterioles.

Hypertensive retinopathy is traditionally graded into four categories. In grade I, there is minimal diffuse or focal narrowing of arterioles. In grade II, "copper" and "silver" wiring (increased light reflex) is evidence of long-standing uncontrolled hypertension. These are considered relatively mild target-organ effects. In grade III and IV retinopathy, cotton-wool spots (focal ischemia), hard exudates and hemorrhages (vessel leakage), and extensive microvascular changes are seen. Grade IV retinopathy is distinguished by disk edema and defines malignant hypertension or hypertensive crisis. (The term papilledema is frequently used, but the disk edema is due to infarction and hypoxia of the optic disk. Thus, the term papilledema is best reserved for disk edema associated with elevated cerebrospinal fluid pressure.) Grade I and grade II retinopathy are evidence of chronic hypertension. Grades III and IV are evidence of accelerated retinopathy particularly in the young. Also grade III and IV changes might not be seen in the elderly. The mechanism of underlying pathology—arteriolar spasm—ultimately leads to degeneration of the muscle of the blood vessel, with subsequent degeneration of the endothelial cells of the vessel lumen. The elderly, who are likely to have arteriosclerotic vessels, are paradoxically protected by the presence of this other pathology.

In the brain, an abrupt, sustained rise in blood pressure exceeding the limits of cerebral autoregulation may be associated with stroke, intracerebral hemorrhage, or hypertensive encephalopathy.6 Vascular injury caused by an abrupt or persistent elevation in blood pressure may result in ischemia or infarction in vulnerable regions of the brain. Intracerebral bleeding from dilated vessels may result in cerebral or subarachnoid hemorrhage. Hypertensive encephalopathy is characterized by marked vasospasm with ischemia, punctate hemorrhages, and increased vascular permeability all leading to cerebral edema (a mechanism similar to retinopathy). This mechanism is different from localized cerebral edema in the area of ischemic stroke caused by emboli or thrombi. An increase in blood pressure may be a physiologic response to maintain adequate cerebral perfusion to areas distal to the occlusion and may not justify classification as a hypertensive emergency.

In the heart, increased afterload occurring after an acute rise in blood pressure results in increased left ventricular wall tension that, in turn, increases myocardial oxygen demand. Angina or myocardial infarction occurs when hypertension causes a decrease in coronary blood flow relative to an increased demand. Pulmonary edema occurs when the sudden increase in MAP results in elevated end-diastolic pressure and decreased end-diastolic filling volume precipitating acute left ventricular failure.

In the kidneys, impaired autoregulation due to elevated blood pressure results in decreased renal perfusion. Decreased renal perfusion stimulates the renin-angiotensin (I and II) cascade, leading to increased vasoconstriction. If this cycle continues, arteriolar necrosis occurs, ultimately leading to renal impairment. Angiotensin II can exacerbate hypertension not only by causing vasoconstriction but also by stimulating aldosterone secretion to promote sodium retention. Sodium retention induces hypertension in susceptible individuals by a variety of mechanisms, including (1) increased sympathetic nervous system activity; (2) decreased response to dopamine; (3) change in calcium and potassium metabolism; (4) resistance to insulin; and (5) inappropriate response of renal vasculature and adrenals to angiotensin II.8

Hypertension is associated with major cardiovascular risk factors such as smoking, hyperlipidemia, diabetes mellitus, age older than 60 years, gender (men and postmenopausal women), obesity, and a family history of cardiovascular disease.1 In addition, dietary sodium excess in salt-sensitive individuals (50 percent of hypertensive patients) can induce hypertension. Although no single cause of hypertension has been identified, a combination of factors such as these are believed to contribute to elevated blood pressure.

Although most cases of hypertension are considered to be essential with no known cause, several specific causes do exist. Of the known causes, renal disease is the most prevalent and includes renal arteriostenosis, fibromuscular disease of the renal arteries, chronic pyelonephritis, and nonspecific glomerulonephritis. Coarctation of the aorta, although uncommon, is also an important cause of secondary hypertension and should be suspected in any patient with the triad of upper extremity hypertension, a systolic murmur best heard over the back, and delayed femoral pulses. Another cause of hypertension is excessive glucocorticoids, seen in Cushing syndrome, but usually due to exogenous steroid therapy. Endogenous overproduction is less common but results from excessive adrenocorticotropic hormone (ACTH) production by a pituitary tumor, ectopic ACTH production by a nonpituitary tumor, or glucocorticoid production by tumors of the adrenal cortex. Pheochromocytomas are tumors that produce catecholamines arising from cells of the sympathetic nervous system (most commonly from the adrenal medulla) and account for fewer than 1 percent of cases of hypertension. The characteristic feature of pheochromocytomas is paroxysms of hypertension associated with palpitations, tachycardia, malaise, apprehension, and sweating.9 Finally, ingestion of foods containing large amounts of tyramine can raise blood pressure by causing release of norepinephrine stored in nerve endings. This normally transient response may become prolonged in patients taking monoamine oxidase (MAO) inhibitors, since these agents block the enzyme that destroys tyramine.

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