From the Guidelines
The answer is (c) aspirin. Aspirin inhibits gastric bicarbonate secretion, which is an important protective mechanism for the gastric mucosa. Bicarbonate secretion by the gastric epithelium creates a protective alkaline layer that neutralizes acid near the mucosal surface. Aspirin, a non-steroidal anti-inflammatory drug (NSAID), inhibits cyclooxygenase enzymes that produce prostaglandins. Prostaglandins actually stimulate bicarbonate secretion, so by blocking their production, aspirin reduces this protective mechanism, as noted in the study on the use of nonsteroidal anti-inflammatory agents, including cyclooxygenase-2 enzyme inhibitors and aspirin 1. This is one of the ways aspirin and other NSAIDs can damage the gastric mucosa and lead to ulcer formation. In contrast, the other options -
- prostaglandins,
- vagal stimulation, and
- gastrin - all promote rather than inhibit bicarbonate secretion, contributing to the stomach's defense mechanisms against acid-induced injury. The inhibition of gastric bicarbonate secretion by aspirin is a key factor in its potential to cause gastrointestinal toxicity, as discussed in the context of COX-1–mediated prostaglandin synthesis and its role in promoting the generation of the gastric mucosal protective barrier 1.
From the FDA Drug Label
Misoprostol has both antisecretory (inhibiting gastric acid secretion) and (in animals) mucosal protective properties NSAIDs inhibit prostaglandin synthesis, and a deficiency of prostaglandins within the gastric mucosa may lead to diminishing bicarbonate and mucus secretion and may contribute to the mucosal damage caused by these agents.
- Prostaglandins (such as misoprostol) increase bicarbonate secretion.
- NSAIDs (such as aspirin) inhibit prostaglandin synthesis, which can lead to diminishing bicarbonate secretion.
- Vagal stimulation and gastrin are not directly mentioned as inhibiting gastric bicarbonate secretion in the provided text.
- The correct answer is (c) aspirin, as it is an NSAID that inhibits prostaglandin synthesis, leading to diminished bicarbonate secretion. 2
From the Research
Inhibition of Gastric Bicarbonate Secretion
The following factors can affect gastric bicarbonate secretion:
- Aspirin: Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) can cause gastrointestinal bleeding and ulcers by inhibiting prostaglandin synthesis, which in turn can affect gastric bicarbonate secretion 3, 4.
- Prostaglandins: Prostaglandins can stimulate gastric bicarbonate secretion, and their inhibition by NSAIDs can lead to a decrease in bicarbonate secretion 5.
- Vagal stimulation: Vagal stimulation can increase gastric bicarbonate secretion, but this effect can be suppressed by proton pump inhibitors 6.
- Proton pump inhibitors: Proton pump inhibitors can affect gastric bicarbonate secretion by inhibiting proton back-diffusion and increasing the permeability of the gastric epithelium 6.
- Gastrin: There is no direct evidence to suggest that gastrin inhibits gastric bicarbonate secretion.
Relevant Studies
Studies have shown that:
- Aspirin and NSAIDs can cause gastrointestinal bleeding and ulcers by inhibiting prostaglandin synthesis 3, 4.
- Proton pump inhibitors can prevent NSAID-induced gastrointestinal lesions 7.
- Indomethacin, an inhibitor of endogenous prostaglandin synthesis, can increase basal gastric acid secretion without affecting gastric bicarbonate secretion 5.
- Prostaglandin analogs, such as misoprostol, can stimulate gastric bicarbonate secretion and prevent NSAID-induced gastrointestinal lesions 3, 4.