last updated 24-06-2024

Blood pressure control

Blood pressure control

Three factors play a prominent role in the regulation of blood pressure: cardiac output (CO), blood volume, and peripheral vascular resistance. This graphic depicts how the blood pressure can be increased.

CO depends on the amount of blood returning to the heart (venous return) and the heart rate.

The venous return depends on the preload or the capacitance of the veins. An increase in blood volume will therefore also increase the CO.

CO is also under control of the sympathetic nervous system, which regulates the heart rate.

The blood volume is regulated by the renin-angiotensin-aldosterone system (RAAS), which is a neurohumoral control. RAAS activation results in an increase in aldosterone and antidiuretic hormone (ADH), which cause Na+ retention and water conservation, respectively. See renin-angiotensin-aldosterone system for a more detailed description of this system.

The peripheral vascular resistance is under control of both the sympathetic nervous system and RAAS.

Atrial natriuretic peptide (ANP) is the important hormone in decreasing blood pressure (not depicted here). ANP is released from the right atrium and increases water and Na+ excretion from the kidneys by blocking aldosterone and aldosterone release. ANP also induces peripheral vasodilation.


Sudden assumption of an upright position from supine position causes an initial decrease in: 


The cardiac output cannot increase indefinitely because


A severe decrease in blood volume (due to trauma) leads to the following:


The amount of blood that is forced out of the heart depends on


Following acute haemorrhage, the following compensatory mechanism occurs: