Bainbridge reflex
From Wikipedia, the free encyclopedia
The Bainbridge reflex is an increase in heart rate due to an increase in the blood volume. Increased blood volume is detected by stretch receptors located in both atria at the venoatrial junctions.
Contents |
[edit] History
A scientist by the name of Francis Arthur Bainbridge reported this reflex in 1915 when he was experimenting on dogs. Bainbridge found that infusing blood or saline into the animal increased heart rate. This phenomenon occurred even if arterial blood pressure did not increase. He further observed that heart rate increased when venous pressure rose high enough to distend the right atrium, but denervation of the vagi to the heart eliminated these effects.
[edit] Control of Heart Rate
The Bainbridge reflex and the baroreceptor reflex act antagonistically to control heart rate. The baroreceptor reflex acts to decrease heart rate when blood pressure rises. When blood volume is increased, the Bainbridge reflex is dominant; when blood volume is decreased, the baroreceptor reflex is dominant.
[edit] Venous Return
As venous return increases, the pressure in the superior and inferior vena cavae increase. This results in an increase in the pressure of the right atrium, which stimulates the atrial stretch receptors. These receptors in turn signal the medullary control centers to increase sympathetic stimulation of the heart, leading to increased heart rate, a.k.a. tachycardia.
Increasing the heart rate serves to decrease the pressure in the superior and inferior vena cavae by drawing more blood out of the right atrium. This results in a decrease in atrial pressure, which serves to bring in more blood from the vena cavae, resulting in a decrease in the venous pressure of the great veins. This continues until right atrial blood pressure returns to normal levels, upon which the heart rate decreases to its original level.
[edit] Atrial Stretch Receptors
In the right atrium, the stretch receptors occur at the junction of the vena cavae. In the left atrium, the junction is at the pulmonary veins. Increasing stretch of the receptors stimulates both an increase in heart rate and a decrease in vasopressin (a.k.a. anti-diuretic hormone) secretion from posterior pituitary. This decrease in vasopressin secretion results in an increase in the volume of urine excreted, serving to lower blood pressure. In addition, stretching of atrial receptors increases secretion of atrial natriuretic peptide (ANP), which promotes increased water and sodium excretion through the urine.
Berne, R., Levy, M., Koeppen, B., & Stanton, B. (2004) Physiology, Fifth Edition. Elsevier, Inc.