The control of arterial blood pressure

Mean arterial blood pressure (ABP)

The principal variable regulated by the cardiovascular system to ensure stable tissue perfusion.

ABP formula

ABP = Cardiac Output (CO) × Total Peripheral Resistance (TPR).

Cardiac output definition

The volume of blood pumped by the heart per minute; determined by heart rate × stroke volume.

Total peripheral resistance (TPR)

The combined resistance to blood flow offered by all systemic arterioles.

Pulse pressure

The difference between systolic and diastolic blood pressure.

Mean arterial pressure estimation

Approximately diastolic pressure + 1/3 of the pulse pressure.

Age-related ABP changes

Mean blood pressure tends to rise with age, and is slightly higher in men between puberty and menopause.

Causes of increased pulse pressure

Reduced arterial compliance (e.g., atherosclerosis) or increased diastolic run-off (e.g., exercise or aortic valve leak).

Why mean ABP is regulated, not systolic or diastolic

Keeping ABP constant allows tissues to control their own blood flow by adjusting local resistance.

High-pressure baroreceptors

Mechanosensitive receptors in the carotid sinus and aortic arch that detect stretch and send signals to the NTS to reduce blood pressure.

Baroreceptor afferent nerves

Carotid sinus → glossopharyngeal nerve

aortic arch → vagus nerve.

Baroreceptor reflex effect

Increased baroreceptor firing inhibits the medullary vasomotor centre, reducing sympathetic output and increasing parasympathetic output.

Low-pressure baroreceptors

Stretch receptors in the atria and pulmonary vessels detecting changes in blood volume.

Arterial chemoreceptors

Sensors in carotid and aortic bodies that detect low O₂, high CO₂, and low pH, and can increase sympathetic activity.

Medullary cardiovascular centre

Integrates baro- and chemoreceptor input to adjust sympathetic and parasympathetic output.

Effect of increased sympathetic stimulation

Vasoconstriction (↑TPR), increased heart rate, increased contractility, and venoconstriction.

Effect of vagal stimulation

Reduces heart rate and therefore reduces cardiac output.

α₁-adrenergic receptors

Mediate vasoconstriction through Gq → IP₃ → Ca²⁺ release.

β₂-adrenergic receptors

Cause vasodilation in skeletal muscle and coronary vessels via Gs → cAMP → PKA.

Why afterload changes don’t strongly affect CO

The Frank–Starling mechanism increases contractility automatically with increased arterial pressure.

Short-term ABP regulation

Neural mechanisms (baroreflex) acting within seconds.

Long-term ABP regulation

Primarily controlled by blood volume via renal mechanisms.

Consequences of baroreceptor dysfunction

Inability to buffer changes in ABP, leading to large swings in blood pressure.

Significance of ABP stability

Ensures adequate perfusion of vital organs even when CO or TPR vary.