Which one of the following is NOT an effect of atropine on the human body?
- A) Cardiac stimulation
- B) Diminished sweating
- C) Mydriasis
- D) Reduction of gastrointestinal tone
- E) Stimulation of gastric secretion***
Gastric secretion Gastric secretion is considered the first significant phase of digestion.
Control of gastric secretion:
The regulation of gastric secretion is a true paradigm of gastrointestinal functioning as a whole and depends on an intricate balance of transmitting chemo with excitatory and inhibitory actions simultaneously. These functions are performed by neural, endocrine, autocrine and paracrine routes. Classically, gastric secretion is divided into three phases: cephalic, gastric and intestinal. Cephalic phase: Even before the food is ingested, the stomach is prepared to receive the bolus through brain centers that respond to visual stimuli, smells, flavors and even thoughts related to food. Enteric neurons that release acetyl choline (act directly on the parietal cell and the enterochromaffin cell) and GRP gastrin-releasing peptide (in the vicinity of G cells release gastrin that activates parietal and main cells) are activated via vagal route. Gastric phase: Quantitatively more important phase.The presence of food in the gastric lumen stimulates chemical and mechanical receptors. This is how amino acids and short chain peptides are able to stimulate the release of gastrin from G cells. Gastric distension triggers receptors that start neurally reflect the release of acetyl choline or GRP. Intestinal phase: This phase provides only a small portion of gastric acid secretion in the presence of food in the intestine. Its mediators are still controversial, among which is the neuropeptide related to the [calcitonin CGRP] gene] which acts on D cells to induce the release of somatostatin. This phase is not fully understood and is thought to serve to sterilize any gastric food remnants and prepare it for the next food.
Gastric juice components:
- Hcl
- parietal cell
- Protein hydrolysis
- Sterilization
- Intrinsic factor
- parietal cell
- Absorption of vitamin B12
- Pepsinogen
- Main cell
- Proteolysis
- HCO3 (Mucus)
- epithelial cell
- Gastroprotection
- Trefoil factors
- Gastroprotection
- Histamine
- Enterochromine cell
- Acid secretion regulation
- Gastrina
- G cell
- Acid secretion regulation
- Somatostatin
- Cell D
- Acid secretion regulation
Physiology of gastric acid secretion:
Basal acid secretion:
In the stomach at rest and on an empty stomach, acid secretion has a diurnal pattern and its proportion varies widely among normal people. Although serum gastrin concentrations do not correlate with basal acid production, the important factors are vagal "tone" and sex. Evidence indicates that a high vagal tone can lead to sustained baseline hypersecretion in some people and temporary hypersecretion during periods of stress in others. Women generally secrete less acid at baseline than men.Stimulated acid secretion:
In the activation of the cellular receptors of the gastric parietal cell 2 mechanisms are involved: one central and one peripheral. The central nervous system integrates sensory information that comes from specialized senses, central chemoreceptors and visceral sensory receptors. Efferent stimulating impulses are transmitted through the vagus nerve to the peripheral neurons of the enteric nervous system.The enteric nervous system integrates information from the vagus, with peripheral sensory information and regulates the release of mediating substances that activate the parietal cell. The most important substances that are released are acetylcholine, by the fibers of the vagus nerve and histamine, by cells similar to the entherochromaffins (ECL). The stimulation of the ECL to release histamine is the major route of regulation for the stimulation of acid secretion by the parietal cell.
The best peripheral mechanism for the regulation of gastric acid secretion is the plasma gastrin level, which is raised by the arrival of food to the antral region (mainly proteins and amino acids) and decreases the level when the secretion of gastrin by an intragastric pH less than 3. in the presence of food, can lead to hypergastrinemia.
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