Physiological mechanisms of gastric acidity and consequences of acid hypersecretion

Physiological mechanisms of gastric acidity and consequences of acid hypersecretion

Gastric acid (HCl) is produced by parietal cells. Its main functions are as follows: to facilitate the digestion of proteins, activating pepsinogen into pepsin; assist the absorption of micronutrients such as iron, calcium and vitamin B12; and reduce the chance of enteric infections and bacterial overgrowth. However, when there is acid hypersecretion related to an imbalance of the aggressive and protective mechanisms of the gastric mucosa, gastric acid-related diseases arise, such as peptic ulcer.

Read too: Long-term use of proton pump inhibitors: myths and truths

How does acid production occur?

The stomach has three anatomical areas: fundus, body and antrum. Functionally, it is divided into two glandular areas:

  • Oxyntic region: corresponds to 80% of the stomach, including fundus and body. The main cell is the parietal, producing HCl.
  • Pyloric Region: corresponds to 20% of the stomach, predominantly in the antrum. The typical cell is the gastrin-producing G cell.

Oxyntic glands are composed of mucous cells, parietal cells (HCl), enterochromafin-like (histamine), D cells (somatostatin), chief cells (pepsinogen) and enterochromafin cells (atrial natriuretic peptide).

The pyloric glands are composed of mucous cells, G cells (gastrin) and D cells (somatostatin).

The production of HCl by parietal cells is regulated by 3 main pathways:

  1. Neurocrine – mainly acetylcholine released by the enteric nervous system;
  2. Endocrine – hormones, such as gastrin;
  3. Paracrine – release of substances such as histamine.

Of these pathways, they are responsible for stimulating gastric secretion:

  • Release of acetylcholine by enteric postganglionic neurons;
  • Gastrin, released by the G cells of the antrum;
  • Histamine, released in the oxyntic glands, by enterochromaffin-like cells.

The main pathway of inhibition of gastric secretion is the release of somatostatin by D cells.

Acid production in parietal cells depends on activation of signaling pathways dependent on cAMP and intracellular calcium, culminating in fusion and activation of the Na pump+/K+ ATPase. In addition to the proper functioning of the proton pump, this production requires the functioning of apical potassium and chloride channels, as well as basolateral chloride and bicarbonate channels.

Know more: Update on the management of refractory gastroesophageal reflux disease

How do proton pump inhibitors inhibit acid secretion?

Proton pump inhibitors (PPIs) are weak bases that, at acidic pH (pH < 4), act by inhibiting the Na pump.+/K+ apical membrane ATPase. To have greater potency, they should be taken 30 minutes before the first meal of the day.

What is the impact of hypergastrinemia?

Gastrin is a hormone responsible for stimulating acid production in parietal cells. Thus, high gastric acidity and somatostatin have negative feedback with gastrin. Similarly, an increased gastric pH induces gastrin production, leading to hypergastrinemia, as, for example, in patients with atrophic gastritis or using PPIs.

It is important to mention that gastrin is a trophic hormone that stimulates the proliferation of mucosa and enterochromaffin cells. Thus, situations that lead to hypergastrinemia, such as atrophic gastritis and Zollinger-Ellison syndrome (gastrin-producing tumor), are related to carcinoid tumors (tumors originating from enterochromaffin cells).

How is acid production after meals?

In basal metabolism, there is a containment of acid secretion through the action of somatostatin on the cells enterochromaffin-like (histamine producing), parietal cells (HCl producing) and G cells (gastrin producing).

When we eat, maximum acid secretion occurs. This occurs because there is removal of inhibition by somatostatin, in addition to direct stimulation of parietal cells and gastrin release. During a meal, there is activation of central neurons, the vagus nerve and the enteric nervous system, promoting the release of acetylcholine. This, in turn, directly stimulates acid production by activating parietal cells, in addition to stimulating gastrin production and inhibiting somatostatin production.

The meal in the stomach acts as a buffer for the acidic environment, raising the pH and contributing to the inhibition of somatostatin. After gastric emptying, the acid secretion containment mechanism is activated again.

What is the relationship between the Helicobacter pylori and acid secretion?

During acute infection with Helicobacter pylori (H. pylori), there is an increase in somatostatin, leading to a reduction in gastrin and hydrochloric acid. In addition, there is direct inhibition of parietal cells by cytotoxins produced by this agent. This reduction in acidity favors the survival of the bacteria, allowing the colonization of the stomach.

In chronic infection by H. pylori it can happen so much hypochlorhydria how much hyperchlorhydria:

  • In 15% of cases, it courses with antral gastritis and reduced somatostatin, causing increased gastric acidity. In this subtype, the occurrence of duodenal ulcers is common;
  • In 85% of cases, it progresses with pangastritis and reduced acid secretion due to functional inhibition of parietal cells by bacterial or inflammatory products. Over time, these patients may develop atrophy of the oxyntic glands (atrophic gastritis).

When is it necessary to measure gastric pH?

Currently, the main role of fasting gastric acidity measurement is in the evaluation of patients with Zollinger Ellison syndrome. The disease progresses with hypergastrinemia, with increased basal acid production.

The most used method to obtain the sample is the aspiration of gastric juice through a nasogastric tube, with the patient fasting. This sample can also be obtained by endoscopic examination. Basal acid production is about 10 mmol of H+ per hour in men and 5 mmol per hour in women.

What are the main conditions associated with increased gastric acid production?

  • Duodenal ulcer (mostly associated with antral infection by H. pylori);
  • Type II and III gastric ulcers;
  • Systemic mastocytosis, which courses with high levels of histamine;
  • Antrectomy with Billroth II anastomosis (exposure to alkaline secretion reducing somatostatin and activating gastrin);
  • Chronic hypercalcemia regardless of etiology (stimulation of gastrin release and activation of parietal cells);
  • Zollinger Ellison syndrome (gastrinoma).

Practical messages

One of the main functions of the stomach is acid secretion, which is important in the digestion process, as well as in protecting against enteric infections. Neural, endocrine, and paracrine mediators regulate this secretion. A deregulation in this production can lead to problems such as peptic ulcer disease.

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