Gastric Motility

Yet another lecture that draws on concepts from previous semesters!

Gastric Smooth Muscle

This lecture started off with some notes about the anatomy. The outermost layer of the gut is the serosa. Beneath the serosa are at least two layers of muscle: an outer longitudinal layer and an inner circular layer. Between these two layers lies the myenteric plexus of nerves that go through the gut. Beneath the muscle layers is the submucosa, which contains the submucosal plexus. Finally, you have the mucosa layer, which is folded into villi in order to increase the surface area.

Next up, this lecture covered depolarisation of smooth muscle, as well as the pathway involved in myosin phosphorylation and contraction. I've covered this here and here. Note that gastric smooth muscle uses pretty much only electromechanical coupling (see here for the details on what that is).

Slow waves and generation of contraction

See previous post: Physiology of Smooth Muscle

Slow waves are also known as BER (Basic Electrical Rhythm), PSP (Pace-Setter Potential) or ECA (Electrical Control Activity). They only have a small amplitude (~10-15mV). The slow wave frequency is at its highest in the duodenum and at its lowest in the stomach.

Slow waves are generated mainly by non-selective cation channels, which allow entry of Na⁺ and Ca²⁺. These channels close when Ca²⁺ accumulates on the inside of the cell, preventing further build-up of positive charge. Mitochondrial and cytoplasmic Ca²⁺ also oscillate in phase with slow waves, and it has been thought that mitochondrial Ca²⁺ may be at least partially responsible for slow waves (since mitochondria remove Ca²⁺ from the cytosol). Interestingly enough, if you get rid of IP₃ receptors, slow waves stop. We still don't know why, though.

As mentioned in the previous post, slow waves do not cause contraction on their own. If they go above threshold at any point, action potentials can occur, and action potentials can cause contraction. Acetylcholine and other parasympathetics can cause depolarisation, making it more likely that the slow waves will cross threshold. Noradrenaline and other sympathetics have the opposite effect: they can cause hyperpolarisation, making it less likely that slow waves will cross threshold. At rest, parasympathetic tone is dominant.

Neural control of motility

The GI tract is fairly well innervated. Most parasympathetic stimulation comes from the vagus, and most sympathetic stimulation comes from the mesenteric ganglia. Most parasympathetic and sympathetic nerves actually go to the enteric nerves, rather than directly to the organs. Enteric neurons show long-acting excitation and inhibition patterns. As mentioned above, stimulation can lead to depolarisation (in the case of parasympathetics) or hyperpolarisation (in the case of sympathetics).

Motility of the stomach

The stomach can be divided into two main regions: the proximal and distal stomach. The proximal stomach has slow, sustained (i.e. tonic) contractions. The distal stomach, on the other hand, has peristaltic (phasic) contractions. The pacemaker is located in between these two sections.

As the stomach becomes full, it relaxes, keeping the pressure constant. This relaxation is not due to a myogenic response, but rather due to vagal reflexes. Another effect of vagal stimulation following stomach distension is that gastric emptying is stimulated. Other stimuli for gastric emptying include stimulation of the gastric nerve plexus by stomach distension, and the hormone gastrin. Gastric emptying can be inhibited by acid, fats, hyperosmotic solutions (e.g. consuming too much salt), and a bunch of hormones, such as secretin and gastric inhibitory peptide.

Motility of the small intestine

The small intestine moves in segmentation (as described here), propulsive waves, and so on. The end result is that the food gets mixed and moved along the intestines. Propulsive waves are coordinated via the myenteric plexus and hormones. Movement is stimulated by the hormones cholecystokinin (CCK), gastrin, insulin, and serotonin, but it is inhibited by secretin and glucagon.