Primary hypertension (HTN) appears to be related to hereditary and environmental factors. While the exact mechanism is unclear, the heritable component of HTN has been documented in familial and twin studies.1 In genetically susceptible persons, environmental factors (dietary sodium, obesity, and stress) appear to increase the likelihood of HTN. Tubular sodium ion concentrations are sensed by specialized cells located in the JGA and signal changes in glomerular filtration rate and renin production.2 Several populations are also known to be prone to salt sensitivity including African-Americans, those with a family history of HTN, the obese, and the elderly.3-6 The JGA also has a dense sympathetic nerve supply and sympathetic activity has also been shown to increase renin synthesis.7
In patients with high BP, defects in sodium transport have also been described.8,9 Abnormal sodium transport across the cell membrane increases intracellular sodium concentrations, which leads to increased intracellular calcium ion concentration and increased vascular smooth muscle sensitivity to sympathetic stimulation. There is also evidence that persons with HTN may have decreased nitric oxide activity, a vasodilating substance produced by endothelial cells.10 The mosaic theory holds that multiple factors sustain elevated BP even though initially only one aberrant factor may have been responsible (Figure 2).11
Moreover, modified by genetic and environmental factors, BP consistently increases with age. Data suggests that individuals with normal BP at 55 years of age have a 90% lifetime risk of developing primary HTN.12
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