Monday 16 January 2006
Hypertension is a common health problem with some-times devastating consequences, and often remains asymptomatic until late in its course. Hypertension is one of the most important risk factors for both coronary artery disease and cerebrovascular accidents; hypertension can lead to cardiac hypertrophy and, potentially, heart failure, aortic dissection, and renal failure.
It is widely acknowledged that hypertension is a complex, multifactorial disease that has both genetic and environmental determinants. Molecular pathways underlying blood pressure variation have been recently elucidated, creating possible targets for therapeutic intervention. Nevertheless, the pathogenic mechanisms of hypertension in the majority of affected individuals remain largely unknown.
The detrimental effects of blood pressure increase continuously as the pressure rises, and no rigidly defined threshold level of blood pressure distinguishes risk from safety. Regardless, a sustained diastolic pressure greater than 90 mm Hg or a sustained systolic pressure in excess of 140 mm Hg is considered to constitute hypertension.
By these criteria, screening programs reveal that 25% of persons in the general population are hypertensive. Hypertension affects more than 800 million individuals worldwide. The prevalence and vulnerability to complications increase with age and, for unknown reasons, are high in African Americans. Epidemiologic data indicate that systolic blood pressure is more important than diastolic blood pressure as a determinant of cardiovascular risk, except in young individuals.
Reduction of blood pressure dramatically reduces the incidence and death rates from IHD, heart failure, and stroke. However, more than one fourth of those with hypertension are not aware that they have the disorder and, in as many as three fourths of those with known hypertension, the condition may be poorly controlled.
A small number of patients (approximately 5%) have underlying renal or adrenal disease (such as primary aldosteronism, Cushing syndrome, pheochromocytoma), narrowing of the renal artery, usually by an atheromatous plaque (reno-vascular hypertension) or other identifiable cause (secondary hypertension).
However, about 95% of hypertension is idiopathic (called essential hypertension). This form of hypertension generally does not cause short-term problems; especially when controlled, is compatible with long life and is asymptomatic, unless a myocardial infarction, cerebrovascular accident, or other complication supervenes. Thus, this subgroup is often called benign hypertension.
A small percentage, perhaps 5%, of hypertensive persons show a rapidly rising blood pressure that if untreated, leads to death within a year or two.
Called accelerated or malignant hypertension, the clinical syndrome is characterized by severe hypertension (i.e., systolic pressure over 200 mm Hg, diastolic pressure over 120 mm Hg), renal failure, and retinal hemorrhages and exudates, with or without papilledema.
It may develop in previously normotensive persons but more often is superimposed on pre-existing benign hypertension, either essential or secondary.
The multiple mechanisms of hypertension constitute aberrations of the normal physiologic regulation of blood pressure. Arterial hypertension occurs when the relationship between cardiac output and total peripheral resistance is altered. For many of the secondary forms of hypertension, these factors are reasonably well understood. For example, in renovascular hypertension, renal artery stenosis causes decreased glomerular flow and pressure in the afferent arteriole of the glomerulus.
This (1) induces renin secretion, initiating angiotensin II-mediated vasoconstriction and increased peripheral resistance, and (2) increases sodium reabsorption and therefore blood volume through the aldosterone mechanism. In pheochromocytoma, a tumor of the adrenal medulla, catecholamines produced by tumor cells cause episodic vasoconstriction and thus induce hypertension.
Regulation of Normal Blood Pressure
Blood pressure is proportional to cardiac output and peripheral vascular resistance. Indeed, the blood pressure level is a complex trait that is determined by the interaction of multiple genetic, environmental, and demographic factors that influence cardiac output and vascular resistance. The major factors that determine blood pressure variation within and between populations include age, gender, body mass index, and diet, principally sodium intake.
Cardiac output is highly dependent on blood volume, itself greatly influenced by the whole body sodium homeostasis. Peripheral vascular resistance is determined mainly at the level of the arterioles and is affected by neural and hormonal factors.
Normal vascular tone reflects the balance between humoral vasoconstricting influences (including angiotensin II, catecholamines, and endothelin) and vasodilators (including kinins, prostaglandins, and NO).
Resistance vessels also exhibit autoregulation, whereby increased blood flow induces vasoconstriction to protect against tissue hyperperfusion. Other local factors such as pH and hypoxia, and the α- and β-adrenergic systems, which influence heart rate, cardiac contraction, and vascular tone, may be important. The integrated function of these systems ensures adequate perfusion of all tissues, despite regional differences in demand.
The kidneys play an important role in blood pressure regulation as follows:
Through the renin-angiotensin system, the kidney influences both peripheral resistance and sodium homeostasis. Renin elaborated by the juxtaglomerular cells of the kidney converts plasma angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme. Angiotensin II raises blood pressure by increasing both peripheral resistance (direct action on vascular SMCs) and blood volume (stimulation of aldosterone secretion, increase in distal tubular reabsorption of sodium).
The kidney also produces a variety of vascular relaxing, or antihypertensive, substances (including prostaglandins and NO), which presumably counterbalance the vasopressor effects of angiotensin.
When blood volume is reduced, the glomerular filtration rate falls, leading to increased reabsorption of sodium by proximal tubules and thereby conserving sodium and expanding blood volume.
Natriuretic factors, including the natriuretic peptides secreted by atrial and ventricular myocardium in response to volume expansion, inhibit sodium reabsorption in distal tubules and thereby cause sodium excretion and diuresis. Natriuretic peptides also induce vasodilation and may be considered to represent endogenous inhibitors of the renin-angiotensin system.
When renal excretory function is impaired, increased arterial pressure is a compensatory mechanism that helps restore fluid and electrolyte balance.
Hypertension not only accelerates atherogenesis but also causes degenerative changes in the walls of large and medium arteries that potentiate both aortic dissection and cerebrovascular hemorrhage.
Malignant hypertension by Washington Deceit
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