Blood pressure is controlled by a combination of your nervous system, hormones, kidneys, and the physical structure of your blood vessels, all working together in real time. At its most basic, blood pressure equals cardiac output (how much blood your heart pumps per minute) multiplied by the resistance your blood vessels create. Everything that raises or lowers blood pressure does so by changing one or both of those variables.
The Nervous System: Second-by-Second Adjustments
Your body has built-in pressure sensors called baroreceptors, located in the walls of your carotid arteries (in your neck) and your aortic arch (just above your heart). These sensors detect how much the artery wall is stretching with each heartbeat and send continuous signals to a control center in your brainstem.
When blood pressure rises, the baroreceptors fire more rapidly, telling the brain to dial back the sympathetic nervous system. This relaxes the walls of small arteries, reducing resistance and letting pressure fall. When blood pressure drops, the opposite happens: baroreceptor firing slows, the brain ramps up sympathetic activity, and your blood vessels constrict while your heart rate increases. This is why you don’t faint every time you stand up. The moment gravity pulls blood toward your legs and pressure in your upper body drops, the baroreceptor reflex kicks in within a beat or two, tightening vessels and speeding up your heart to compensate.
The Hormonal Cascade: RAAS
For longer-term pressure control, your body relies on a hormonal chain reaction called the renin-angiotensin-aldosterone system, or RAAS. It starts in the kidneys. When blood pressure falls or blood flow to the kidneys drops, specialized kidney cells release an enzyme called renin into the bloodstream. Renin breaks apart a protein made by the liver, producing angiotensin I. Then, an enzyme in the lungs and kidneys converts angiotensin I into angiotensin II.
Angiotensin II is one of the most powerful blood-pressure-raising substances in your body. It narrows the walls of small arteries, directly increasing resistance. It also triggers your adrenal glands to release aldosterone and signals your pituitary gland to release antidiuretic hormone (vasopressin). Together, these hormones tell your kidneys to hold onto sodium and water, expanding blood volume and pushing pressure higher. Most common blood pressure medications work by interrupting one or more steps in this cascade.
Hormones That Lower Blood Pressure
Your body doesn’t just have an accelerator for blood pressure. It also has a brake. When blood volume rises and stretches the walls of your heart’s upper chambers, the heart releases a hormone called atrial natriuretic peptide, or ANP. ANP does essentially the opposite of RAAS: it relaxes blood vessel walls, increases the rate at which your kidneys filter blood, and blocks sodium reabsorption. This causes you to excrete more sodium and water, reducing blood volume. ANP also directly suppresses renin release, shutting down the RAAS cascade at its source.
People with lower ANP levels tend to have higher aldosterone levels, which helps explain why some individuals are more prone to high blood pressure than others.
Vasopressin: Water Retention and Vessel Tightening
Antidiuretic hormone (vasopressin) raises blood pressure through two simultaneous mechanisms. In the kidneys, it triggers the insertion of water channels into the cells lining the collecting ducts, allowing water to flow back into the bloodstream instead of being excreted as urine. In blood vessels, it directly causes smooth muscle to contract, increasing resistance. These two effects are synergistic: more fluid in the system plus tighter vessels means a meaningful rise in pressure. This hormone is especially important during dehydration or blood loss, when maintaining adequate blood flow to organs becomes critical.
Your Kidneys: The Long-Term Regulator
While the nervous system handles moment-to-moment fluctuations and hormones manage changes over hours, your kidneys are the ultimate long-term regulator of blood pressure. They do this through a process called pressure natriuresis. When blood pressure rises, increased pressure in the kidney’s blood vessels causes the kidneys to excrete more sodium and water, bringing blood volume and pressure back down. When pressure drops, the kidneys retain more sodium and water.
This mechanism acts as a reset switch. Even if every other system in the body is pushing pressure higher, the kidneys can gradually bring it back toward normal by shedding excess fluid. But when the kidneys themselves are impaired, or when the hormonal signals telling them to retain sodium are too strong, this safety valve fails, and chronic high blood pressure develops.
How Salt Intake Affects the System
High sodium intake forces the body to retain extra water to keep sodium concentrations in the blood stable. This expands blood volume, increases cardiac output, and raises the pressure flowing through your arteries. In a healthy system, the kidneys respond by ramping up sodium excretion until a new balance is reached. But not everyone’s kidneys respond with the same efficiency. In people who are “salt-sensitive,” the kidneys are slower to excrete the excess, and blood pressure stays elevated longer or permanently. Roughly 18 of the 21 genes most strongly linked to primary hypertension involve salt-sensitive pathways.
Blood Vessel Stiffness and Aging
Your arteries aren’t rigid pipes. In a young, healthy person, the large arteries near the heart are elastic. They stretch when the heart pumps and recoil between beats, smoothing out blood flow and keeping pressure relatively steady. This elasticity matters because it stores some of the energy from each heartbeat and releases it during the resting phase, helping maintain blood flow to organs even between beats.
With age, the walls of these large arteries gradually stiffen and lose their ability to stretch. This has a specific and predictable effect on blood pressure readings. Before about age 50, both the top number (systolic) and bottom number (diastolic) tend to rise together, driven mainly by increased resistance in smaller blood vessels. After 50, something shifts. Diastolic pressure plateaus and then begins to fall, while systolic pressure keeps climbing. The gap between the two numbers, called pulse pressure, widens. This happens because stiff arteries can no longer absorb the force of each heartbeat. Pressure waves also travel faster through rigid arteries and bounce back sooner, arriving while the heart is still pumping rather than after it relaxes, which adds even more force to the systolic reading.
This is why isolated systolic hypertension, where the top number is high but the bottom number is normal or low, is overwhelmingly a condition of older adults.
Genetics and Heritability
Blood pressure has a strong genetic component. Heritability estimates range from 25% to 60%, meaning a substantial portion of the variation in blood pressure between people is explained by inherited genes rather than lifestyle alone. Researchers have identified at least 21 genes with strong evidence of contributing to primary hypertension. Most of these genes influence how the kidneys handle sodium, how the RAAS hormonal system is regulated, or how blood vessel walls respond to pressure. If high blood pressure runs in your family, your threshold for developing it is likely lower, and the lifestyle factors that affect pressure (salt intake, weight, physical activity) carry more weight for you.
Current Blood Pressure Categories
The 2025 guidelines from the American Heart Association and American College of Cardiology define four categories based on readings taken in a clinical setting:
- Normal: below 120/80 mm Hg
- Elevated: systolic 120 to 129, diastolic below 80
- Stage 1 hypertension: systolic 130 to 139, or diastolic 80 to 89
- Stage 2 hypertension: systolic 140 or higher, or diastolic 90 or higher
If your systolic and diastolic numbers fall into two different categories, the higher category applies. These thresholds reflect the pressure levels at which cardiovascular risk begins to climb meaningfully and at which intervention changes outcomes.