Positive Feedback Mechanisms

In positive feedback mechanisms, the result or response enhances the original stimulus so that the activity (output) is accelerated. This feedback mechanism is “positive” because the change that occurs proceeds in the same direction as the initial disturbance, causing the variable to deviate further and further from its original value or range. In contrast to negative feedback controls, which maintain some physiological function or keep blood chemicals within narrow ranges, positive feedback mechanisms usually control infrequent events that do not require continuous adjustments. Typically, they set off a series of events that may be self-perpetuating and that, once initiated, have an amplifying or waterfall effect. Because of these characteristics, positive feedback mechanisms are often referred to as cascades (from the Italian word meaning “to fall”). Positive feedback mechanisms are likely to race out of control, and so they are rarely used to promote the moment-to-moment well-being of the body. However, two familiar examples of their use as homeostatic mechanisms are the enhancement of labor contractions during birth and blood clotting.

The positive feedback mechanism in which oxytocin, a hypothalamic hormone, intensifies labor contractions during the birth of a baby is described in Chapter 28 (see Figure 28.16). Oxytocin causes the contractions to become both more frequent and more powerful. The increased contractions cause more oxytocin to be released, which causes more contractions and so on until the baby is finally born, an event that ends the stimulus for oxytocin release and shuts off the positive feedback mechanism.

Blood clotting is a normal response to a break in the lining of a blood vessel and is an excellent example of an important body function controlled by positive feedback. Basically, once vessel damage has occurred, blood elements called platelets immediately begin to cling to the injured site and release chemicals that attract more platelets. This rapidly growing pileup of platelets initiates the sequence of events that finally forms a clot.