Peristaltic Reflex: Function, Tasks, Role & Diseases

The peristaltic reflex is a movement reflex in the intestine. The reflex is triggered by pressure on mechanoreceptors located in the intestine. The nervous system of the intestine is relatively autonomous, so the reflex can still be observed in an isolated intestine. In diseases such as diabetes, the reflex may cease.

What is the peristaltic reflex?

The peristaltic reflex is a movement reflex in the intestine. The reflex is triggered by pressure on mechanoreceptors located in the intestine. The movements of the intestine are referred to as peristalsis. Different movement patterns of peristalsis are distinguished. For example, the so-called pacemaker cells of the intestine control slow potential waves every second or minute. During digestion, non-propulsive peristalsis occurs in the form of annular contractions. Transport of intestinal contents toward the rectum occurs via propulsive peristalsis. Continuous contractions of different intestinal areas prevent the upward migration of the intestinal contents. The peristaltic reflex is the triggering of the characteristic intestinal peristalsis by a stretching stimulus. Physiologically, the intestinal contents provide the stretching stimulus to trigger the digestive movements. The fuller the intestine becomes, the more the intestinal contents stimulate the so-called mechanoreceptors of the intestinal mucosa. When a threshold potential is exceeded, the enterochromaffin cells in the intestinal walls secrete serotonin. This is a messenger substance of the enteric nervous system. The serotonin excites the nerve cells of the intestinal wall and thus triggers muscle contractions or relaxations. Because of the neurotransmitter, the reflex is independent of the central nervous system and can also be observed in the isolated intestine.

Function and task

In the human organism, there are several nervous systems that act relatively independently of each other. In addition to the central nervous system, the autonomic nervous system should be mentioned. Together with the sympathetic and parasympathetic nervous systems, the enteric nervous system forms the autonomic system. The enteric nervous system is the autonomic nervous system of the gastrointestinal tract, which is similar in structure to the brain. For this reason, the gastrointestinal tract is also called the small brain. Extrinsic sympathetic and parasympathetic nerve pathways monitor and regulate intestinal motor activity, but ultimately the gastrointestinal tract is the only organ still capable of functioning in isolation from the central nervous system. All motor activity of the anatomical structure is thus controlled quasi autonomously. The enteric motor activity is a reflex motor activity. Consequently, digestion is involuntary and independent of the patient’s own decisions. The maintenance of all digestive movements is the task of the enteric nervous system. For communication purposes, enteric neurons synthesize more than 25 transmitter substances. More than 1,000 different transmitter combinations are thus theoretically available to control gastrointestinal motor activity. Approximately 30 populations function as sensory neurons, motoneurons, and interneurons and harbor neurotransmitters. The main mode of function of the enteric nervous system is synaptically mediated activation and inhibition. Fast excitatory postsynaptic potentials are among the most important transmission mechanism. Acetylcholine is the primary neurotransmitter in the enteric nervous system. It activates postsynaptic neurons by binding to nicotinic receptors. Serotonin and adenosine triphosphate also participate in mediation. Serotonin binds to 5-HT3 receptors. The enteric nervous system regulates its effector systems through reflex circuits. The peristaltic reflex thereby shapes propulsive peristalsis. The IPAN (intrinsic primary afferent neurons) in the enteric nervous system are stimulated by the mechanical pressure of the intestinal contents or by chemical stimuli, and initiate a reflex circuit that causes higher-level contraction and lower-level relaxation of the circular muscles. Projection polarity of enteric motor neurons ensures functioning. Inhibitory and excitatory motor neurons can be directly targeted by the IPAN. However, the IPANs can also use an intermediate interneuron for indirect activation. The circuitry proceeds over distances of millimeters to centimeters. Several of these circuits are activated immediately one after the other.Its modulation is given to the transport of intestinal contents by synaptic contacts between circuit elements receiving activation or inhibition.

Diseases and disorders

Pathologic hyperactivity of inhibitory neurons in the intestine causes the intestinal muscles to relax to such an extreme that there is near atony. In extreme cases, the peristaltic reflex comes to a standstill. Even complete paralysis of the intestine can occur in this way. The peristaltic reflex can then no longer be triggered. The resident mechanoreceptors no longer register any stimuli, even in the presence of strong intestinal wall tension. The opposite condition can also have disease value, for example, in the case of pathological hyperactivity of the excitatory system. Such hyperactivity results in accelerated transit and diarrhea. Many diseases of the intestine are accompanied by functional obstruction. Some of these diseases arise on the basis of neuronal degeneration, which can take different degrees. For example, generalized degeneration affects the inhibitory and excitatory nerve cell populations of the enteric nervous system. When the inhibitory nerves fail, the consequences are more severe than a failure of the excitatory cells. The inhibitory neurons of the intestine maintain a braking effect on intestinal movement. Complete loss of inhibitory tone can result in conditions such as Hirschsprung’s disease, achalasia, or stenosis of the sphincters. Any of these diseases may be rooted in local aganglionosis. Hypoganglionosis results in intestinal pseudoobstruction. These associations play a role, for example, as causes of dysfunction in Chagas disease and cytomegalovirus infection. Diabetes mellitus can also disrupt enteric circuits. In this case, the dysfunctions are manifested mainly by slowed gastric emptying, which may increase to apparent paresis. Neurological diseases such as multiple sclerosis attack the central nervous system rather than the enteric system. All associated bowel dysfunction has sympathetic or parasympathetic causes and does not lie in the bowel itself.