Blood pressure is regulated throughout the day in response to changes in body position, movement, pain, temperature, mood and emotion. Short-term methods of regulation exert control over blood pressure in seconds through to hours, whilst long-term regulatory methods act over days, weeks and months to influence future blood pressure function.

Short-term regulation

There are a variety of neural and humoral (hormonal) mechanisms that act in the short term to control blood pressure. These mechanisms have the ability to change blood pressure almost instantly to meet the needs of the body.

Neural Mechanisms

Muscles in the walls of blood vessels, primarily arteries, are controlled by the nervous system. When activated by nerves, the muscular walls contract, causing vasoconstriction of the arteries. Vasoconstriction narrows the diameter of the artery, thus decreasing the amount of blood that can flow through the vessel. This increases the resistance to blood flow through the artery, which increases the blood pressure inside the artery.

Two types of nervous system receptors are involved with the neural mechanisms of short-term blood pressure response: baroreceptors and chemoreceptors. Baroreceptors are located in the wall of the heart and the blood vessels and measure the amount of stretch in the vessel walls. As the amount of stretch decreases, the baroreceptor activates and tells the brain to trigger the nerves that control the muscles in the artery walls, thus causing vasoconstriction and an increase in blood pressure. This is most commonly experienced when changing your body position rapidly from lying down to sitting or standing. As you stand up, blood is redistributed around the body, causing a decrease in the tension (or stretch) on the blood vessel walls. The baroreceptors sense this change and activate the nervous system to cause vasoconstriction. This creates an almost-instant increase in blood pressure to ensure that blood continues to circulate properly around the body as you change positions.

Chemoreceptors are receptors located in the aorta (the body’s main artery) and the carotid arteries (the arteries that deliver blood to the brain). They measure the oxygen, carbon dioxide and hydrogen levels in the blood as it moves through the arterial system. The primary role of chemoreceptors is to measure the rate of ventilation (how quickly we breathe), however as blood pressure decreases, blood flow through the circulatory system can become impaired. This causes a decrease in the oxygen content of the blood and an increase in the carbon dioxide and hydrogen levels in the blood – these changes are detected by the chemoreceptors. The chemoreceptors then tell the brain to activate the nerves that control the muscles of the artery walls, thus causing vasoconstriction and an increase in blood pressure.

Humoral Mechanisms

The humoral mechanisms involved in short-term regulation of the blood vessels include the renin-angiotensin-aldosterone system (RAA) and vasopressin.

The RAA system is an integral component of both short-term and long-term regulation of blood pressure. Renin is an enzyme created in the kidneys in response to decreases in blood pressure, fluid volume (hydration) and/or sodium (salt) concentration. Most of the renin created in the kidneys is released into the blood stream and is ultimately converted into into angiotensin II at the lungs. Angiotensin II causes vasoconstriction of the arteries, thus assisting with the short-term regulation of blood pressure. Angiotensin II also stimulates the release of aldosterone from the adrenal glands – aldosterone increases both sodium (salt) and fluid retention in the kidneys, which acts on increasing blood volume. Fluid retention and blood volume are important mechanisms in the long-term regulation of blood pressure.

Vasopressin is a hormone released from the pituitary gland in response to decreases in blood volume and blood pressure. It acts on the blood vessels to cause vasoconstriction, thus increasing blood pressure in the short term. Vasopressin is also called the antiduretic hormone and works on the kidneys to inhibit fluid release, thus promoting fluid retention in the body. The effects of fluid retention on blood pressure will be discussed in the next session, however the fluid retention role of vasopressin is also thought to exert control over blood pressure regulation in the short term.

Long-term regulation

The short-term mechanisms to control blood pressure are not effective when required over a considerable period of time. Instead, the kidneys play an active role in maintaining blood pressure over the course of the day, week, month and longer.

Blood pressure is closely related to hydration levels. As hydration levels rise, blood volume increases. This requires the heart to contract more forcefully to push blood through the circulatory system – these more forceful heart contractions increase the resistance to blood flow through the arteries, which increases blood pressure. Therefore, the kidneys can act to increase blood pressure when required by retaining fluid rather than releasing it in urine. This is achieved by releasing vasopressin to promote water retention and releasing renin to spark the RAA system. As a result, angiotensin II is created, which stimulates the release of aldosterone. Aldosterone acts of the kidneys to promote water retention, hence increasing blood volume and, ultimately, blood pressure.

When an increased blood pressure needs to be restored to a more normal level, the kidneys facilitate a release of fluid. This release of fluid decreases the blood volume, which decreases the workload on the heart and decreases the resistance to blood flow through the arteries, thus causing a drop in blood pressure. Fluid loss is achieved by reducing the rate of renin secretion. This inhibits the RAA system and slows the creation of angiotensin II and aldosterone. As angiotensin II levels fall, vasodilation of the arteries occurs – this increases the amount of blood that can flow through the artery and decreases the resistance to blood flow, resulting in a decrease in blood pressure. A drop in angiotensin II levels also causes a fall in aldosterone levels. At the same time, vasopressin release is also slowed or inhibited. The combined fall in both aldosterone and vasopressin levels reverses the fluid retention activities of the kidneys and promotes fluid loss. (It should be noted that as the kidneys facilitate fluid release, the released fluid is stored in the bladder prior to being eliminated through urination. This gives the kidneys the opportunity to constantly change the amount of water to be released during the day and filter small amounts of water gradually out of the body without needing frequent toilet stops!)

The short-term and long-term mechanisms are effective in controlling blood pressure in healthy individuals. However, in cases of hypertension, there is a breakdown in either the short-term and/or long-term mechanisms that control blood pressure. The next part of this series will examine how certain lifestyle factors, like diet and smoking, can influence the development of hypertension and other potential hypertensive-related disorders.

References

Mayet, J. & Hughes, A. (2003). Cardiac and vascular pathophysiology in hypertension. Heart, 89(9), pp. 1104-1109.

Porth, C.M. (2009). Disorders of blood pressure regulation. In C.M. Porth & G. Matfin (Eds). Pathophysiolgy: Concepts of altered health states. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins.