The Physiology of slow waves

Pacemaker of GIT is Located in – Slow Waves Arise From Interstitial Cells of Cajal

Concerning the origin of the slow waves, studies show that slow waves originate in specialized smooth muscle cells called interstitial cells of Cajal. Interstitial cells of Cajal are interconnected to form complex networks of specialized smooth muscle fibers that lie between the smooth muscle layers. Moreover, the interstitial cells make synaptic-like connections with GI smooth muscle fibers. The cyclic changes in membrane potential of interstitial cells of Cajal are due to the presence of unique ion channels, which spontaneously open, and close. The opening of these unique channels creates inward currents, which may generate a slow wave.

The electrical signals that arise in the ICC spread quickly into adjacent GI smooth muscle cells through gap junctions. Thus, interstitial cells of Cajal act in similar fashion to myocardial autorhythmic cells.

Interstitial cells of Cajal are in close association with enteric neurons making it easy for the enteric neurons to control the activities of the ICC.

Although the ICC sends impulses for basic GI smooth muscle contraction, neurotransmitters, hormones, and paracrine modulators modify the force and duration of contraction of GI smooth muscles.

Normally, slow waves on their own are unable to cause GI smooth muscle contraction, rather they act as pacemaker currents that excite the appearance of spike potentials. Slow wave potentials result in spike potentials (true action potentials) and contraction only when they reach threshold value.

GI smooth muscle cells have an unstable resting membrane potential of -50mV to -60mV. If the slow wave potential rises above -40mV, spike potentials appear superimposed on the slow wave.

Another feature of the spike potential is that the higher the amplitude of the slow wave (i.e. the higher the slow wave rises), the higher the frequency of spike potentials. The frequency of spike potential normally ranges from two (2) to ten (10) spikes per second.

Ionic Basis of GI Smooth Muscle Action Potential

Concerning the ionic basis of action potentials in GI smooth muscle, the ion channels responsible for the spike potentials are not the fast sodium channels, which occur in nerve fibers. Rather, the ion channels responsible for action potentials in GI smooth muscle cells are different. In nerve fibers, action potential result entirely from the opening of fats sodium ion channels whereas action potentials in GI smooth muscle cells result from the opening of special ion channels called calcium-sodium channels.

The calcium-sodium channels allow for the significantly large amount of calcium ions to enter together with a significantly smaller amount of sodium ions. Perhaps, this is why we call them calcium-sodium ion channels. Compared to the fast sodium channels of nerve fibers, calcium-sodium channels are slower to open and close.

The slow manner in which these channels open and close makes action potentials of GI smooth muscles to last much longer than that of nerve fibers. Normally, action potentials (spike potentials) of GI smooth muscles last as long as 12 to 20 milliseconds which is about 10 to 40 times as long as action potentials in large nerve fibers.

Slow waves that reach threshold potential cause voltage-gated calcium (Ca2+) in the smooth muscle fibers to open allowing calcium ions to enter the muscle fiber cells. The influx of calcium ions triggers the muscle fiber cells to fire one or more action potentials.

The depolarization phase of the GI smooth muscle action potential, much the same with that of myocardial pacemaker cells, occurs due to calcium ions entry into the GI smooth muscle cell.

Once again, note that slow waves occur due to the opening of sodium ion channels and entry of only sodium ions into the GI smooth muscle (calcium ions channels fail to open during slow wave). Calcium ions fail to take part in slow waves, for this reason, slow waves by themselves are unable to trigger muscle contractions. Rather, it is during spike potentials (which are true action potentials that enough amounts of calcium ions enter the smooth muscle fibers to cause contraction.

Spike Potential of GI Tract – Action Potentials

Slow waves can generate action potentials only when they reach threshold voltage. Slow wave that are below threshold voltage are unable to generate action potential (spike potentials) whereas slow waves that reach threshold voltage results in spike potentials.

Slow waves occur due to opening of fast sodium ion (Na+) channels whereas spike potentials occur due to the opening of slow calcium-sodium ion (Ca2+-Na+) channels. However, more calcium ions than sodium enter the smooth muscle during the depolarization phase of spike potentials. Repolarization occurs after depolarization and is due to potassium ion efflux.

Note that smooth muscles of the esophagus and proximal segment of the stomach are unable to show these spontaneous rhythmic fluctuations in membrane potentials.

Stretch, Ach, Parasympathetic Stimulation and GI Hormones can Alter RMP and Consequently the Basic Electrical Rhythm of GI Smooth Muscles

Recall that the resting membrane potential of GI smooth muscle fibers ranges from -50mV to -60 mV, and that under normal physiologic conditions, the resting membrane potential of GI smooth muscle averages -56mV. Nevertheless, multiple factors can alter this basal voltage level. Changes in the RMP that makes the RMP more positive and less negative called depolarization effects make the GI smooth muscle to be more excitable whereas changes that make the RMP more negative and less positive called hyperpolarization effect make the GI smooth muscle less excitable.

A depolarized GI smooth muscle is more excitable and responds to excitatory stimulus with greater ease. In contrast, a hyperpolarized GI smooth muscle is less excitable and responds to excitatory stimulus with difficulty.

Among the principal factors that can increase the BER of GI smooth muscles making them to be more excitable, include:

  1. Stretch or distention of GI smooth muscles
  2. Effect of acetylcholine on the membrane of the GI smooth muscle
  3. Stimulation by parasympathetic nerves which release acetylcholine at their nerve endings
  4. Finally stimulation by some GI hormones

These factors increase both the frequency of spikes (and contraction) as well as the force of contraction.

Among the important factors that can decrease the BER of GI smooth muscles making them to be less excitable, include:

  1. Stimulation of sympathetic nerve, with consequent release of norepinephrine mainly
  2. Effect of norepinephrine or epinephrine on the membrane of the GI smooth muscle

Above-mentioned factors decrease both the frequency of spikes (and contractions) as well as the force of contraction.

Pacemaker frequency differs between different regions of the gut with the duodenum having the highest and the cecum having the least.

BER in various regions of the GIT

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6 thoughts on “The Physiology of slow waves

  1. Thanks for combing all of these good points. I see that you mentioned Ca++ is responsible for the rising phase of the AP.

    However, is it mentioned what ions are responsible for establishing slow-wave potentials? I want to know what ions are causing the autorhythmic cycles of depolarization and repolarization that make up the the digestive tracts basic electrical rhythm.

    • Hi Rebecca,
      Slow waves (also called BER) are oscillating depolarization and repolarization of membrane potential of GI smooth muscle cells.
      Cyclical opening of Na+ and the entrance of Na+ into GI cells causes the depolarization phase of basal electrical rhythm (BER); whereas, cyclical opening of K+ channels, and the exit of K+ causes the repolarization phase

  2. Hi, i wanted to ask that are spike potentials generated when the GIT is in resting state. I mean when there is no external stimulus and a certain part of GIT is completely empty of food, will the slow waves cross the threshold of -40 and cause spike potentials

  3. Hello Khizar,

    First, understand that for spikes to be generated from slow waves, there must be a stimulus.
    Certain part of the GI tract undergo contraction in the absence of food. This inter-digestive contractions in the small intestine is called Migrating Motor Complex. It is triggered by the GI hormone called motilin.
    Thus, the small intestine undergo spike potentials and contraction even in the absence of food. However, the GI hormone called motilin is responsible for this contraction. In the absence of motilin, this contractions would cease.

    Second, even when the GI tract is empty, the wall still maintains a mild tonic contraction. This tone is due to basal parasympathetic discharge and influx of minute quantities of Calcium ions into the GI smooth muscle cells.

    Need more help. Feel free to send me a mail at

  4. Hello, thank you very much for this well-explained post.
    i just wanted to know the relation between slow waves, spike potentials and peristaltic contraction this seems to confuse me a bit ! and is the frequency of contration that of slow waves?

    • Hi Faz, Resting membrane potential of GI smooth muscles averages about -50 to -60 milliVolts. Slow waves are not contractions but rhythmical alterations in membrane potential caused by variations in sodium conductance. They occur due to complex interactions among the smooth muscle cells and specialized cells, interstitial cells of Cajal – pacemaker cells. Slow waves fire action potentials (also called spike potentials) when they reach threshold, about -40 mV. Spikes are true action potentials that cause GI smooth muscle contractions. The frequency of slow waves depends on the segment of the digestive tract – in the small intestine, they occur 10 to 20 times per minute and in the stomach and large intestine 3 to 8 times per minute. You could find out more on slow waves in this post

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