Hypertension:Etiology
Causes Of Hypertension
Essential or idiopathic hypertension is systemic hypertension of unknown cause and accounts for 90-95% of hypertension cases. Essential hypertension is known to cluster within families. Genomic research has revealed that the genetic component of essential hypertension is polygenic in nature. Investigations are under way to identify the particular genes involved; associated genes identified to date include the angiotensinogen gene and the alpha-adducin gene. The remaining 5-10% of hypertension cases (known as secondary hypertension) have an identifiable cause such as renal insufficiency, endocrine abnormalities, or monogenic (single-gene) inherited forms of high blood pressure.
Ethnic and Gender Variations
Ethnicity and gender are important in the pathogenesis of hypertension. In the United States, hypertension is more common in the black population than in the white population, and the prevalence and incidence of hypertension are slightly greater in men than in women. This gender difference is more apparent in the young and middle-aged (those younger than age 60) and reverses in the elderly population.
Hypertension Risk Factors
Sodium Intake
Increased dietary sodium is associated with increased blood pressure and is therefore viewed as a key risk factor for the development of hypertension. Circumstantial evidence indicates that hypertensive animals and people, as well as their offspring, have higher levels of intracellular sodium than nonhypertensives.
Potassium Intake
Most epidemiological studies point to an inverse relationship between potassium intake and high blood pressure. However, controversy surrounds the association between low serum potassium levels and the hypertension disease process; further studies are required.
Body Mass
The relationship between body mass and blood pressure is well established. Large interventional trials revealed a reduction in the incidence of hypertension and in systolic blood pressure and diastolic blood pressure following a reduction in body weight. The mechanism by which obesity contributes to hypertension risk is unclear, but it may involve excessive calorie intake, perhaps with coincident sodium intake and retention, or an altered sensitivity to insulin that can contribute to obesity. Dietary alterations and exercise leading to weight loss can help reduce blood pressure; unfortunately, there is a trend toward more sedentary lifestyles.
Birth Weight
An increasing body of evidence points to a link between birth weight and blood pressure in adult life. Babies who are smaller than average at birth are more likely to have higher blood pressure during adolescence, culminating in the development of hypertension in adulthood. The mechanisms behind this phenomenon remain to be established.
Alcohol Consumption
A close relationship exists between alcohol consumption and hypertension. Moderate to high alcohol consumption is associated with raised blood pressure and increased risk of potentially fatal cardiovascular events. Studies demonstrate a decrease in both systolic blood pressure and diastolic blood pressure following reduced alcohol consumption. However, mild alcohol consumption is commonly associated with decreased arterial pressure; nondrinkers commonly display slightly higher blood pressure measurements than do mild to moderate drinkers. Research suggests that alcohol consumption should be limited to 1 ounce per day in men and 0.5 ounce in women and people of lesser weight.
Smoking
As with other risk factors, the link between smoking and the risk of developing hypertension has long been established. blood pressure remains elevated for 15 minutes after a person finishes smoking a cigarette. Cigarette smoking increases oxidative stress within the vasculature, leading to increased adhesion molecule expression on the endothelial cell layer and decreased nitricoxide (NO) bioavailability, ultimately resulting in endothelial dysfunction. A recent study by Dutch researchers that involved 2,412 nonsmokers, 2,704 former smokers, and 1,508 current smokers found that smoking interacts with polymorphisms of the angiotensin-converting enzyme gene in a way that increases the risk of developing hypertension. These findings highlight the significance of the interaction between genetic and environmental factors in this disease.
This post has been viewed 721 times.
Comments are closed.
