Which of the following inhibits gastric bicarbonate secretion: (a) prostaglandins (PG), (b) vagal stimulation, (c) aspirin (acetylsalicylic acid), or (d) gastrin?

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Which Agent Inhibits Gastric Bicarbonate Secretion?

Aspirin (c) inhibits gastric bicarbonate secretion, which is a key protective mechanism of the gastric mucosa. 1

Mechanisms of Gastric Protection and NSAID-Induced Damage

Role of Prostaglandins in Gastric Protection

  • Prostaglandins play a crucial protective role in the gastric mucosa by stimulating the synthesis and secretion of mucus and bicarbonate, as well as promoting epithelial proliferation and increasing mucosal blood flow 2
  • Prostaglandins found in the stomach have dual protective effects: they inhibit acid secretion and enhance mucosal defensive mechanisms 3
  • Endogenous prostaglandins modulate acid secretion and stimulate both mucus and bicarbonate secretion in the stomach and duodenum, serving as key components of the mucosal defense system 3

How Aspirin Inhibits Bicarbonate Secretion

  • Aspirin decreases both basal and prostaglandin-stimulated bicarbonate secretion in the duodenum through histamine-dependent and histamine-independent pathways 1
  • Aspirin causes topical injury to the mucosa and systemic effects through prostaglandin depletion, which impairs the gastric mucosal protective barrier 2
  • The inhibition of prostaglandin synthesis by aspirin leads to reduced bicarbonate secretion, creating an environment more susceptible to acid-peptic damage 1, 4

Effects of Other Agents on Bicarbonate Secretion

Prostaglandins (option a)

  • Rather than inhibiting bicarbonate secretion, prostaglandins actually stimulate bicarbonate secretion in the gastroduodenal mucosa 2, 5
  • Prostaglandins of the E type have been shown to enhance protective mechanisms including bicarbonate secretion 5
  • A prostaglandin-depleted mucosa (as occurs with NSAID use) is more susceptible to damage due to impaired bicarbonate secretion 3

Vagal Stimulation (option b)

  • There is no evidence in the provided literature that vagal stimulation inhibits gastric bicarbonate secretion
  • The vagus nerve is primarily associated with stimulation of gastric acid secretion, not inhibition of bicarbonate secretion 2

Gastrin (option d)

  • None of the evidence provided indicates that gastrin inhibits gastric bicarbonate secretion
  • Gastrin is primarily known for its role in stimulating gastric acid secretion 2

Clinical Implications of Aspirin's Effect on Bicarbonate Secretion

  • The inhibition of bicarbonate secretion by aspirin contributes to its ulcerogenic potential, especially when used chronically 2
  • Even low-dose aspirin (81-325 mg/day) used for cardiovascular protection increases the risk of GI injury through these mechanisms 2
  • Attempts to coat or buffer aspirin have not successfully mitigated these GI effects, as the systemic inhibition of prostaglandin synthesis still occurs 2

Protective Strategies

  • Proton pump inhibitors (PPIs) can be used as co-therapy to reduce the risk of aspirin-induced gastric damage 2
  • H2-receptor antagonists may provide some protection against aspirin-induced duodenal ulcers but are less effective for gastric ulcers 2
  • Patients with risk factors such as age over 60-65 years, history of GI bleeding, or concurrent use of multiple antithrombotics should receive gastroprotection when taking aspirin 6

In conclusion, among the options presented, only aspirin (c) inhibits gastric bicarbonate secretion, which is an important mechanism contributing to its potential for causing gastroduodenal injury.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Role of endogenous prostaglandins in gastric secretion and mucosal defense.

Clinical and investigative medicine. Medecine clinique et experimentale, 1987

Research

Dual COX inhibition and upper gastrointestinal damage.

Current pharmaceutical design, 2003

Research

Prostaglandins: effects on the gastrointestinal tract.

Clinical physiology and biochemistry, 1984

Guideline

Management of Patients on Long-Term PPI and SAID Therapy

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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