Archives of Digestive Disorders

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Perspective - Archives of Digestive Disorders (2025) Volume 7, Issue 1

Gastric acid secretion: Regulation, mechanisms, therapie

Gianrico Farrugia*

Department of Gastrointestinal motility, Mayo Clinic, USA

*Corresponding Author:
Gianrico Farrugia
Department of Gastrointestinal motility
Mayo Clinic, USA.
E-mail: Farrugia@wustl.edu

Received : 09-Jan-2025, Manuscript No. AAADD-25-189; Editor assigned : 13-Jan-2025, PreQC No. AAADD-25-189(PQ); Reviewed : 31-Jan-2025, QC No AAADD-25-189; Revised : 11-Feb-2025, Manuscript No. AAADD-25-189(R); Published : 20-Feb-2025 , DOI : 10.35841/ aaadd-7.1.189

Citation: Farrugia G. Gastric acid secretion: Regulation, mechanisms, therapie. Arch Dig Disord. 2025;07(01):189.

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Introduction

The complex process of gastric acid secretion is critically important for nutrient digestion and maintaining the body’s defenses against pathogens. Precise regulation of acid output is achieved through a finely tuned interplay of various physiological factors. This article clarifies histamine's essential role in prompting gastric acid release. It details how histamine, through H2 receptors on parietal cells, acts as a primary stimulant, driving the proton pump [1].

Understanding this fundamental mechanism is key to developing effective acid-suppressing therapies. This review provides a comprehensive overview of how gastric acid is secreted and tightly regulated. It highlights the complex interplay of neural, hormonal, and paracrine factors that control parietal cell function, emphasizing the importance of precise acid output for digestion and host defense [2].

This regulation ensures optimal conditions for digestion while also providing a crucial barrier against ingested pathogens. This article sheds new light on gastrin's regulatory effects on gastric acid secretion. It explains how gastrin, primarily by stimulating enterochromaffin-like cells to release histamine, orchestrates a potent acid response, a central component of the digestive process [5].

Gastrin's actions underscore a central component of the digestive process, demonstrating how hormonal signals effectively amplify the acid response. This systematic review investigates the intertwined roles of cholinergic and histaminergic pathways in controlling gastric acid secretion. It emphasizes that acetylcholine and histamine are primary stimulators, often working synergistically to modulate acid output, a crucial insight for understanding digestive physiology [4].

The synergistic behavior of acetylcholine and histamine provides crucial insights for understanding broader digestive physiology and identifying potential therapeutic targets. This paper details the critical physiological roles of somatostatin in the stomach, particularly its inhibitory effects on gastric acid secretion. It elucidates how somatostatin acts as a powerful brake, directly on parietal cells and indirectly by inhibiting histamine and gastrin release, maintaining acid homeostasis [6].

This powerful inhibitory action helps to maintain critical acid homeostasis, preventing potential damage from excessive acidity. This report explores the protective roles of prostaglandins in the gastrointestinal tract, including their ability to inhibit gastric acid secretion. It highlights how these lipid mediators reduce acid output, enhance mucus and bicarbonate production, and promote mucosal blood flow, collectively guarding against acid-induced damage [7].

These protective functions are vital for guarding against acid-induced damage and preserving mucosal integrity. This paper offers fresh perspectives on how proton pump inhibitors (PPIs) regulate gastric acid secretion. It delves into the molecular mechanisms by which PPIs irreversibly inhibit the H+/K+-ATPase, underscoring their efficacy in acid-related disorders and discussing potential resistance mechanisms [3].

The molecular mechanisms of PPIs, specifically their irreversible inhibition of the H+/K+-ATPase, highlight their profound efficacy in managing various acid-related disorders. This review details the action mechanism of potassium-competitive acid blockers (P-CABs) on gastric acid secretion. It explains how P-CABs directly and reversibly inhibit the H+/K+-ATPase, offering a new generation of potent and rapid acid suppressants compared to traditional PPIs [8].

This newer generation of acid suppressants offers distinct advantages in terms of speed and potency compared to their predecessors. This article explores the intricate connection between the gut-brain axis and gastric acid secretion. It highlights how central nervous system signals, modulated by various neurotransmitters, influence the vagal nerve and enteric nervous system, thereby regulating parietal cell activity and acid output [9].

The complex interplay between central nervous system signals, the vagal nerve, and enteric nervous system showcases a sophisticated level of regulation. This paper investigates ghrelin's multifaceted role in regulating gastric function, including its impact on acid secretion. While primarily known for appetite stimulation, ghrelin also influences acid output, suggesting a complex interplay with other regulatory hormones in maintaining gastric homeostasis [10].

Ghrelin's influence emphasizes that gastric acid control is intricately integrated within broader physiological systems that govern appetite and metabolism. A thorough understanding of these diverse pathways, from direct cellular stimulation and inhibition to broader neural and hormonal influences, is paramount for comprehending digestive physiology and for advancing effective therapeutic strategies against acid-related conditions.

Conclusion

Gastric acid secretion is a precisely controlled physiological process, vital for effective digestion and robust host defense against pathogens. Central to this regulation are primary stimulators such as histamine, which acts through H2 receptors on parietal cells to drive the proton pump, a key target for acid-suppressing therapies. Gastrin also orchestrates a potent acid response, primarily by stimulating enterochromaffin-like cells to release histamine. Cholinergic pathways, with acetylcholine, often work synergistically with histaminergic mechanisms to modulate acid output, highlighting their intertwined roles in digestive physiology. Counterbalancing these stimulatory actions are crucial inhibitory factors. Somatostatin acts as a powerful brake, both directly on parietal cells and indirectly by inhibiting histamine and gastrin release, thereby maintaining acid homeostasis. Prostaglandins provide protective effects within the gastrointestinal tract by reducing acid output, enhancing mucus and bicarbonate production, and promoting mucosal blood flow, which collectively guards against acid-induced damage. Pharmacological interventions leverage these insights; proton pump inhibitors (PPIs) irreversibly inhibit the H+/K+-ATPase, while potassium-competitive acid blockers (P-CABs) offer a new generation of potent and rapid acid suppression through reversible inhibition. Moreover, systemic influences like the gut-brain axis, modulated by various neurotransmitters, regulate parietal cell activity, and ghrelin's multifaceted role further suggests a complex hormonal interplay in gastric function.

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