High blood pressure, also known as hypertension, is 1 of the most well-known major risk factors for cardiovascular disease (CVD) and stroke. Estimates reported by the American Heart Association indicate that in 2007–2010, 33% of all adults aged ≥20 years in the United States had hypertension. Dietary interventions, in particular those based on sodium or potassium intakes, have demonstrated their ability to reduce blood pressure in humans. Two recently published meta-analyses reported that lower sodium intake resulted in lower levels of blood pressure.
Metabolic disorders, such as obesity and non-insulin-dependent diabetes mellitus, and cardiovascular disorders, such as essential hypertension, congestive cardiac failure and atherosclerosis, have two features in common, namely relative resistance to insulin-mediated glucose uptake and vascular endothelial dysfunction. Significant increases in limb blood flow occur in response to systemic hyperinsulinaemia, although there is marked variation in the results due to a number of confounding factors, including activation of the sympathetic nervous system. Local hyperinsulinaemia has a less marked vasodilator action. Insulin may stimulate endothelial nitric oxide production or may act directly on vascular smooth muscle via stimulation of the Na+-H+ exchanger and Na+/K+-ATPase, leading to hyperpolarization of the cell membrane and consequent closure of voltage-gated Ca2+ channels. Skeletal muscle blood flow is a determinant of glucose uptake so endothelial dysfunction, resulting in a relative inability of mediators, including insulin, to stimulate muscle blood flow, may be the underlying mechanism accounting for the association of hypertension with insulin resistance. A complex interaction between endothelial dysfunction, abnormal skeletal muscle blood flow and reduced insulin-mediated glucose uptake is central to the link between insulin resistance, blood pressure, impaired glucose tolerance and the risk of cardiovascular disease.
Osteoporosis is closely connected with hypertension. One of the important function of the bone is a metabolic function as a storehouse for calcium. In osteoporosis, this second function of the bone is also lost, because there is less space available for calcium storage. Calcium deficiency becomes more and more pronounced as we age, due to a reduced calcium intake, poorer intestinal absorption, lower 1,25(OH)2 vitamin D levels because of shorter solar exposure and declining renal function. Secondary hyperparathyroidism would be an unavoidable consequence of aging unless sufficient calcium and/or vitamin D were provided. Since excess PTH removes calcium from bone by stimulating bone resorption, bone mass decreases leading to osteoporosis. In addition, calcium entering soft tissues such as blood vessels and brain, especially the intracellular compartment, may cause functional deterioration of these organs causing hypertension, arteriosclerosis and senile dementia.
The kidney and vasculature are rich sources of NADPH oxidase–derived ROS, which under pathological conditions play an important role in renal dysfunction and vascular damage. Strong experimental evidence indicates that increased oxidative stress and associated oxidative damage are mediators of renovascular injury in cardiovascular pathologies. Increased production of superoxide anion and hydrogen peroxide, reduced nitric oxide synthesis, and decreased bioavailability of antioxidants have been demonstrated in experimental and human hypertension.