Blood pressure is affected by changes in cardiac output, total blood volume, and resistance to blood flow. Cardiac output is the volume of blood that the heart pumps each minute, which can be calculated by multiplying the heart rate (beats/min) times the stroke volume (mL/beat). Peripheral resistance is the resistance to blood flow that occurs in all vessels as blood moves from the heart. It is caused by friction of blood against vessel walls. It is proportional to blood vessel radius, vessel length, and blood viscosity. Mean arterial blood pressure is the product of cardiac output and peripheral resistance. Blood pressure increases or decreases proportionally to changes in these factors. Mechanisms that regulate blood pressure thus are aimed at altering heart rate, peripheral resistance, and stroke volume.
Blood pressure is under both chemical and neural regulation. Chemical regulation involves several hormones that influence blood pressure in a variety of ways. Epinephrine and norepinephrine increase blood pressure by increasing cardiac output. Antidiuretic hormone stimulates water retention, raising blood pressure. Atrial natriuretic peptide increases kidneys' sodium excretion, reducing blood volume and pressure. In contrast, aldosterone promotes kidneys' sodium retention, increasing blood volume and pressure. Angiotensin II is a vasoconstrictor that raises blood pressure. Neural control of blood pressure is exerted over blood vessels by the vasomotor center in the brain stem's medulla oblongata, which is found right above the spinal cord. It integrates three types of autonomic reflexes. Baroreflexes are negative feedback responses triggered by blood pressure changes. Chemoreflexes are responses to changes in blood chemicals such as pH or O2 and CO2 concentrations. The medullary ischemic reflex is the increase in heart rate, contraction force, and vasoconstriction triggered by decreased blood perfusion, or the delivery of oxygenated blood, in the brain.