Hypertension, the most common cardiovascular disease, is diagnosed through repeated measurements of elevated blood pressure. Its risks, including damage to the kidney, heart, and brain, are directly proportional to blood pressure levels. Starting from 115/75 mm Hg, the risk of cardiovascular disease doubles with each increment of 20/10 mm Hg. The diagnosis relies on blood pressure measurements, not on patient symptoms, as hypertension is often asymptomatic until end-organ damage is imminent or already occurred.

Primary hypertension has no identifiable cause, while secondary hypertension has a specific etiology. Elevated blood pressure is typically linked with increased resistance to blood flow through arterioles, with normal cardiac output. It is believed to be caused by multiple abnormalities, with contributory factors including genetic influences, psychological stress, and dietary factors such as high salt intake and low potassium or calcium intake.

Physiologically, blood pressure is regulated by the cardiac output and peripheral vascular resistance. This regulation occurs at the arterioles, postcapillary venules, heart, and kidneys. Baroreflexes, mediated by autonomic nerves, alongside humoral mechanisms, coordinate function at these points to maintain normal blood pressure.

Baroreflexes are accountable for rapid adjustments in blood pressure, reacting to events that lower arterial pressure. The kidney's control of blood volume is pivotal for long-term blood pressure control. When renal perfusion pressure reduces, it triggers the reabsorption of salt and water and renin production, which initiates the renin-angiotensin-aldosterone system (RAAS). It leads to the synthesis of angiotensin II, causing direct vasoconstriction and stimulating aldosterone production. Aldosterone increases renal sodium absorption and intravascular blood volume. Vasopressin also helps maintain blood pressure through its ability to regulate water reabsorption by the kidney.