Acute alcohol use is known to cause transient rises in blood pressure. However, if consumed chronically, alcohol may cause hypertension by mechanisms which are still debated.
Higher concentrations of serum sodium creates an osmotic gradient, which increases intravascular volume and fluid retention.
Excess cholesterol may result in atherosclerosis, or the deposition of cholesterol plaques along arterial walls. As arterial walls thicken and luminal narrowing occurs, the pressure within the vessels increases.
Obesity commonly coexists with hypertension. It is suggested that patients who suffer from both conditions have impaired pressure-natriuresis regulation.
Hypertension has a higher prevalence in black populations than those of other races.
As we age, our blood vessels, especially the aorta, become more stiff and lose elasticity which leads to increased blood pressure.
While the mechanism is still unclear, it is hypothesized that Vitamin D helps to regulate the renin-angiotension-aldosterone system which is involved in blood pressure modulation.
Over time, kidneys may undergo subtle damage via vasoconstriction while regulating acute changes in blood pressure, leading to renal ischemia. Patients with reduced nephron number are more susceptible to this ischemic damage. As more nephrons become dysfunctional, hypertension may develop.
In patients with diabetes, the basement membrane of their blood vessels undergoes non-enzymatic glycosylation, which causes protein build-up within the vessel wall in a process known as hyaline arteriolosclerosis. Vessel lumens become narrowed due to the thickened walls, which causes blood pressure to rise.
Physical activity is recommended to help patients lower their blood pressure. People who exercise regularly are also less likely to be obese and have other comorbidities which are associated with hypertension.
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