Parietal cells, also known as oxynic cells, are more in the neck and body of the gland.This cell is large and mostly conical.The nucleus is round and deeply stained, in the middle, and may have two nuclei;The cytoplasm is homogeneous and obviously eosinophilic.Under the electron microscope, there is an internal secretory canaliculus with tortuous branches in the cytoplasm of parietal cells, and the wall and the top surface of cellsplasma membraneThey are connected and have microvilli.The parietal cells are from the stomachAcid secreting glandParietal cellultrastructural：microvilli, cell endocrine tubule, nucleus.
Parietal cells, also known as oxynic cells, are located in the neck of the gastric gland and protrude into the gland cavity.When not stimulated, there are many tubular vesicles in the cytoplasm of the cervical mucus cell, and there are secretory tubules at the top and many microvilli on the inner wall. When stimulated, the secretory tubules in the cell immediately form a dense network and the tubular wall cellular vesicles disappear.There are many microvilliActinComposed of microfilaments, hydrochloric acid is secreted from the top surface of tubules as an active transport process, which requires a lot of endocrine cells, and this energy is provided by mitochondria in the parietal cells[1]。
There are three kinds ofExocrine gland: Cardiac gland, acid secreting gland and pyloric gland, of which the gland of acid secreting gland mainly consists of parietal cellsMain cellAnd neckMucous cell, parietal cells can secrete hydrochloric acid andInternal factor。There are smooth surface tubules and vesicles around the secretory tubules, calledmicrotubuleThe membrane structure of the vesicular system is the same as that of the cell top and secretory tubules.
This specific structure of parietal cells is significantly different in different secretory phases of cells.In the non secretory phase, the secretory tubules are mostly different fromFundus gland of stomachThe lumen is connected, and the tubule is connected to the top surface of the cellmicrovilliShort and sparse, but the microtubule system is extremely developed;In the secretory phase, the secretory tubules open, the microvilli increase and become longer, and fill the lumen of the secretory tubules, making the free surface of the cells expand about 5 times, while the number of tubules in the microtubule vesicle system decreases dramatically.This shows thatmicrotubuleThe vesicle system is actually the reserve form of the membrane of the secretory tubule.There are a lot of parietal cellsmitochondrionAnd other organelles are less.
Mammalian parietal cells can be stimulated by different secretory factors throughSecond MessengertransductionH/K-ATPase secretes H/K-ATPase encapsulated by HCl. The energy released by hydrolysis of ATP grade chain is used to transport the intracellular H+out of the cell in one direction and the extracellular K into the cell.K cannot passCytoplasmic granuleMembrane, but exists inCell secretionmicrotubuleIn, by having Cl channel andKClK and Cl - are discharged from the cell through the co transport pathway of H/K-ATPase, and then K is recycled into the cell through H/K-ATPase, and H is secreted into microtubules at the same time.Only stomach H/K-ATPase has this unique structure andexchanging mechanismAnd only gastric H/K-ATPase can reduce the intraluminal pH below 4.Cl channel is a component of H/K-ATPase function.
Various types of gastrointestinal tractEffectorCellular and neurotransmitter releasingNerve endingsThere are a variety of receptors in the.In addition to traditional cholinergicgastrin、histamineH2 and other receptors also existProstaglandin EReceptor subtypesSomatostatinReceptor subtypesInterleukin-1Receptor subtypes and other receptors.The secretion function of parietal cells can beacetylcholine, gastrin, histamineH2 receptorAny ofReceptor antagonistBlocked.The histamine H2 receptor is a 70 kDaglycoprotein, with 7 transmembrane domains/G proteincoupling Receptor structure.Histamine is produced bygastric mucosacell surfaceHistamine H2 receptorMediation, ActiveAdenylate cyclaseThe cAMP produced by it plays a key role in opening the Cl channel on the membrane associated with H/K-ATPase.acetylcholine receptorandgastrinReceptor function is mediated by Ca,Prostaglandin E2Through participating in the action of adenylate cyclase on histamine activationAntagonismSecretory function.Gastrin receptor and acetylcholine receptor are not only expressed in parietal cells, but also expressed in secretionSomatostatinD cells and histamine secreting ECL cells.
ECL cellsG cellD cells are the main cells in the stomachSecretory cell, in the peripheral part of parietal cells, through stimulation or inhibitionParacrineEndocrine and neurogenic pathways regulate gastric acid secretion.The integration of these three cell functions is the initial factor determining the degree of stimulation of parietal cells.Gastrin CCK-B receptor activation, bAdrenergic receptorActivated, and some ECL cellsacetylcholine receptorActivates to regulate the function of ECL cells upwards.Gastrin andacetylcholineThis results in the generation of a typical two-phase Ca signal.SomatostatinInteraction with somatostatin type 2 receptorhistamineIt interacts with histamine type 3 receptor and peptide PYY to inhibit the release of histamine from ECL cells and inhibit Ca signal.ECL cells activated Cl channel, K channel, voltage dependent Ca channel and receptor operated Ca channel after stimulation.D cells can begastrinOr CCK activation, it can also be inhibited by acetylcholine and somatostatin.G cellCan beacetylcholineAnd gastrin releasing peptide (GRP), and can also be inhibited by somatostatin.
Sensitivity of parietal cells to gastrin
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Gillen et al. took DU (Hp+), healthy volunteers (Hp -) and healthy volunteers (Hp;The results showed that the gastrin sensitivity values of the first two groups were not statistically significant. The serum gastrin concentration of the third group was significantly higher, and the sensitivity of the third group was significantly lower than that of the other two groups (p<0.0003);MAO in DU group was higher than that in other two groups of healthy volunteers.The conclusion is that the gastrin sensitivity of Hp (+) sexual healthy volunteers is reduced, and the maximum acid secretion energy of DU patients is increased, which has a causal relationship with the hypergastrinemia caused by Hp.Hypergastrinemia caused by Hp infection may have many mechanisms worth exploring.
In order to remove the interference caused by the excessive number of parietal cells and ECL cells in DU patients, Hurlimann et al. studied non ulcer patients;Divide into two groups according to Hp (+) and Hp (-), and observe theirchronic gastritisPentapeptide gastrin - gastric juice analysis and dietary stimulation - plasma gastrin release;The results showed that Hp (+) gastritis was significant (high score, significant);Other BAO (basic gastric acid secretion), PAO (peak gastric acid secretion), MAOPentagastrinED50 (half effective dose) and plasma gastrin value were not different between the two groups;There was no consistency with gastritis score;However, the main finding is that the PALO and MAO of lip (+) patients have considerable variation, and more than 50% of cases are higher or lower than the lower value range of lip (-) patients.The conclusion is that in non ulcer patients, gastritis caused by Hp (+) does not regularly increase MAO, nor does it affect the sensitivity of parietal cells to gastrin;Therefore, lip infection may not be responsible for the increase of these indicators of DU;This paper believes that MAO may be strengthened or weakened in some specific groups of people with chronic lip infection.When considering BAO, MAO and serum gastrin levels of ulcer disease and chronic gastritis in the literature, it is emphasized to pay attention to the scope and extent of gastritis, and the extent to which it may damage parietal cells, G cells, and even ECL cells, so as to avoid unilateral[2]。
