Acid production in the stomach is a vital physiological process that plays a crucial role in digestion, protection against pathogens, and nutrient absorption. The stomach produces hydrochloric acid (HCl) in response to various stimuli, including the presence of food, gastrin hormone release, and neural signals.
1. Mechanism of Acid Production:
The production of hydrochloric acid in the stomach is primarily regulated by parietal cells, also known as oxyntic cells, located in the gastric glands of the stomach lining. The following steps outline the mechanism of acid production:
Stimulation:
Acid production is initiated by neural and hormonal signals in response to the anticipation or ingestion of food. These signals trigger the release of gastrin hormone from G cells in the stomach lining, as well as acetylcholine neurotransmitter release from vagus nerve endings.
Activation of Parietal Cells:
Gastrin and acetylcholine bind to specific receptors on the surface of parietal cells, activating intracellular signaling pathways that increase intracellular calcium levels.
Proton Pump Activation:
Increased intracellular calcium levels stimulate the activity of an enzyme called H+/K+ ATPase, also known as the proton pump, located in the membrane of parietal cells. The proton pump actively transports hydrogen ions (protons) from the cytoplasm into the lumen of the stomach in exchange for potassium ions.
Chloride Secretion:
To maintain electrochemical neutrality, chloride ions (Cl-) are transported into the lumen of the stomach by a chloride channel called the cystic fibrosis transmembrane conductance regulator (CFTR) protein. This process involves the exchange of bicarbonate ions (HCO3-) from the stomach lumen for chloride ions.
Formation of Hydrochloric Acid:
In the stomach lumen, hydrogen ions (H+) and chloride ions (Cl-) combine to form hydrochloric acid (HCl), a strong acid with a pH ranging from approximately 1.5 to 3.5.
2. Regulation of acid production through the parasympathetic nervous system
The parasympathetic nervous system plays a crucial role in regulating acid production in the stomach by stimulating gastric acid secretion through neural pathways. Parasympathetic innervation of the stomach originates from the vagus nerve (cranial nerve X), which releases the neurotransmitter acetylcholine to activate parietal cells in the gastric glands. The regulation of acid production through the parasympathetic nervous system involves several steps:
1. Stimulation of Vagus Nerve:
Parasympathetic stimulation of acid production begins with the activation of the vagus nerve, which sends nerve impulses to the stomach in response to various stimuli, including the sight, smell, taste, and anticipation of food.
2. Release of Acetylcholine:
Nerve endings of the vagus nerve release the neurotransmitter acetylcholine onto parietal cells and other cells in the gastric mucosa.
3. Activation of Parietal Cells:
Acetylcholine binds to muscarinic acetylcholine receptors on the surface of parietal cells, triggering intracellular signaling pathways that increase intracellular calcium levels.
4. Stimulation of the Proton Pump:
Increased intracellular calcium levels activate an enzyme called H+/K+ ATPase, also known as the proton pump, which is located in the membrane of parietal cells. The proton pump actively transports hydrogen ions (protons) from the cytoplasm into the lumen of the stomach in exchange for potassium ions.
5. Secretion of Hydrochloric Acid:
As hydrogen ions are transported into the stomach lumen, chloride ions (Cl-) are also transported into the lumen through a chloride channel called the cystic fibrosis transmembrane conductance regulator (CFTR) protein. This process creates an acidic environment in the stomach lumen, leading to the formation of hydrochloric acid (HCl).
6. Stimulation of Other Gastric Secretions:
Parasympathetic stimulation not only activates acid secretion but also stimulates the release of other gastric secretions, including pepsinogen from chief cells and mucus from mucous cells, which contribute to the digestion and protection of the gastric mucosa.
