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Hypertension can be divided into two types: essential (or primary) hypertension and secondary hypertension. If hypertension is caused by other diseases and the high blood pressure is gone after these diseases are cured, then the hypertension is the secondary hypertension. If hypertension is not caused by other diseases, it is the essential hypertension.
The causes of essential hypertension are not fully understood. However, it is known that salt plays an important role. Eating foods with more salt will increase the risk of developing hypertension. It also depends on the genes involved in processing salt intake. A more detailed explanation is given below.
Blood pressure = Cardiac output x Systemic vascular resistance
where the "cardiac output" is the blood volume pumped by the heart per minute and the "systemic vascular resistance" is the resistance of the blood vessels to blood flow. The two factors are regulated by complex systems such as renin-angiotensin-aldosterone system, baroreceptors, natriuretic peptides, kinin--kallikrein system, adrenergic receptor system, and others. However, the major pathway leading to essential hypertension is surprisingly simple. It turns out that salt plays the central role.
The Major pathway to hypertension
When there is excess salt in the body, the blood volume increases, because the amount of water must increase to maintain plasma sodium concentration at a constant level. This is accomplished by two mechanisms: (1) Excess salt increases the osmolality of the body fluids, thereby stimulating the thirst center to make the person drink more water. (2) The increase in osmolality also causes the release of antidiuretic hormone, which makes the kidneys to reabsorb water before it is excreted as urine. Since the blood pressure is proportional to the cardiac output (and the blood volume), this explains why excess salt should increase the blood pressure.
In addition to the direct relationship with blood pressure, cardiac output can also affect blood pressure indirectly through "autoregulation". Higher cardiac output triggers autoregulation mechanism to constrict blood vessels all over the body. Increased vasoconstriction also raises blood pressure.
Kidney and salt
The amount of salt in the body is mainly controlled by kidneys, which filter over 170 liters of plasma containing 23 moles of sodium daily. More than 99 percent of the filtered sodium are reabsorbed at four locations: (1) the proximal tubule of the nephron (by Na+/H+ exchange), (2) the thick ascending loop of Henle (by Na-K-2Cl cotransport), (3) the distal convoluted tubule (by Na-Cl cotransport), and (4) the cortical collecting tubule (by epithelial sodium channels) (Figure). Gene mutations that increase salt reabsorption will raise blood pressure.
The epithelial sodium channels at the last location are tightly regulated by the renin-angiotensin-aldosterone system. Renin is an enzyme that can convert angiotensinogen into angiotensin I. The latter can further be converted into angiotensin II by angiotensin converting enzyme (ACE). Angiotensin I is inactive but angiotensin II can stimulate the secretion of aldosterone, which then binds to the mineralocorticoid receptor, triggering a series of events that lead to the increase of epithelial sodium channel activity. Higher sodium channel activity will increase salt reabsorption, thereby causing higher blood pressure. On the other hand, angiotensin II can cause blood vessels to constrict, which also increases blood pressure. Inhibition of ACE can prevent the production of angiotensin II, thus lowering blood pressure. ACE inhibitors have been widely used to control hypertension.