Physiology of Blood Pressure Control
Physiology of Blood Pressure Control
The body’s blood pressure is a measure of the pressures within the cardiovascular system during the pumping cycle of the heart. The blood pressure or systemic arterial pressure refers to the pressure measured within large arteries in the systemic circulation. Each heartbeat forms a pressure wave that travels down the arterial system. The peak of the wave occurs during systole when blood is under pressure from cardiac contraction making the arterial wall expand. During diastole when the heart is briefly relaxing-the arterial walls recoil, delivering a pulse. Systemic circulation provides oxygenated blood to all organs in the body. After perfusing the organs, blood is returned to the right atrium of the heart through the systemic venous system (Lowry, 2016).
Cardiac output is a major factor determining blood pressure, however, as blood flows into the arterial system it meets resistance (in the form of friction) from contact with blood vessel walls. The main resistance to blood flow occurs in the arterioles, which are smaller vessels formed from the branching of arteries (Lowry, 2016). Resistance from all blood vessels in the systemic circuit combines to produce the systemic vascular resistance, which increases blood pressure in the systemic arterial system. These two factors together cardiac output and the systemic vascular resistance, generate actual blood pressure in the systemic arterial system (Lowry, 2016).
Overactivity of the Sympathetic Nervous System (SNS)
Decreased arterial pressure is detected by baroreceptors, which trigger a sympathetic response. This stimulates an increase in heart rate and cardiac contractility leading to increased blood pressure. The sympathetic nervous system serves as the final common pathway for controlling the smooth muscle tone of the blood vessels. Most of the sympathetic preganglionic fibers that control vessel function originate in the vasomotor center of the brain stem and travel in the intermediolateral column of the spinal cord and exit with the ventral nerves; they then synapse with postganglionic fibers in the paravertebral ganglia. Increasing sympathetic activity causes constriction of some vessels, such as those of the skin, gastrointestinal tract, and kidneys (Porth, 1998).
Overactivity of the Renin-Angiotensin-Aldosterone System (RAAS)
The renin-angiotensin-aldosterone system is an essential regulator of arterial blood pressure. The system relies on several hormones that act to increase blood volume and peripheral resistance. It begins with the production and release of renin from juxtaglomerular cells of the kidney. They respond to decreased blood pressure, sympathetic nervous system activity, and reduced sodium levels within the distal convoluted tubules of the nephrons. In response to these triggers, renin is released from the juxtaglomerular cells and enters the blood where it comes in contact with angiotensinogen which is produced continuously by the liver.
The angiotensinogen is converted into angiotensin I by renin. The angiotensin I then make its way to the pulmonary vessels, where the endothelium produces the angiotensin-converting enzyme (ACE). Angiotensin I is then converted to angiotensin II by ACE (Shahoud et al., 2020). Angiotensin II is a potent vasoconstrictor. It acts directly on the kidney to increase sodium reabsorption in the proximal convoluted tubule. Sodium is reabsorbed via the sodium-hydrogen exchanger. Angiotensin II also promotes the release of aldosterone (Lowry, 2016).
