Parietal cells histamine-2 receptor

The parietal cell contains receptors for gastrin (CCK-B), histamine (H2), and acetylcholine (muscarinic, M3) (Figure 62-1). When acetylcholine (from vagal postganglionic nerves) or gastrin (released from antral G cells into the blood) bind to the parietal cell receptors, they cause an increase in cytosolic calcium, which in turn stimulates... 

Parietal cells possess receptors for three stimulators of acid secretion neural (acetylcholine, muscarinic-type receptor), paracrine (gastrin) and endocrine control (histamine, H2 type receptor) (Figure 4.2). 

The stomach secretes hydrochloric acid under the influences of vagus nerve stimulation, gastrin and histamine. Histamine is the most potent stimulus of gastric acid secretion in some animal species studied, such as the horse (Kitchen et al 1998a). Histamine is released by mast cells and enterochromaffin-like cells that are immediately adjacent to the parietal cells. Histamine interacts with two distinct subsets of histamine H2 receptors on the parietal cell membrane, initiating a series of reactions that result in the phosphorylation of protein kinases and increased intracellular calcium within the parietal cell. This, in turn, results in transformation and translocation of the... 

The histamine H2-receptor (359 amino acids) is best known for its effect on gastric acid secretion. Histamine H2-receptor activation, in conjunction with gastrin and acetylcholine from the vagus, potently stimulate acid secretion from parietal cells. High concentrations of histamine are also present in cardiac tissues and can stimulate positive chronotropic and inotropic effects via H2-receptor stimulation and activation of adenylyl... 

Histamine (B). Histamine is stored in basophils and tissue mast cells. It plays a role in inflammatory and allergic reactions (p. 72, 326) and produces bronchoconstriction, increased intestinal peristalsis, and dilation and increased permeability of small blood vessels. In the gastric mucosa, it is released from enterochromaffin-like cells and stimulates acid secretion by the parietal cells. In the CNS, it acts as a neuromodulator. Two receptor subtypes (G-pro-tein-coupled), H and H2. are of therapeutic importance both mediate vascular responses. Prejunctional H3 receptors exist in brain and the periphery. 

Ib. Inhibitors of add production. Acting on their respective receptors, the transmitter acetylcholine, the hormone gastrin, and histamine released intra-mucosally stimulate the parietal cells of the gastric mucosa to increase output of HCl. Histamine comes from entero-chromaffin-like (ECL) cells its release is stimulated by the vagus nerve (via Mi receptors) and hormonally by gastria The effects of acetylcholine and histamine can be abolished by orally applied antagonists that reach parietal cells via the blood. 

Histamine receptors on parietal cells belong to the H2 type (p. 114) and are blocked by H2-antihistaniines. Because histamine plays a pivotal role in the activation of parietal cells, H2-anti-histamines also diminish responsivity to other stimulants, e.g gastrin (in gas-2000 Thieme... 

Histamine also evokes a copious secretion of highly acidic gastric juice from the gastric glands at doses below those that influence blood pressure (32). This effect of histamine is mediated through 2 receptors on the parietal cells. The importance of this effect in scombroid poisoning is not knowi. Histamine also has some stimulant actions on salivary, pancreatic, intestinal, bronchial, and lacrimal secretions (32), but these effects are relatively unimportant. 

H2-receptor antagonists are drugs used to block the action of histamine on parietal cells in the stomach, decreasing acid production by these cells. These drugs are used in the treatment of dyspepsia however, their use has waned since the advent of the more effective proton pump inhibitors. 

C. Histamine stimulates gastric acid secretion through an effect on Hj-receptors of gastric parietal cells. Although certain antihistamines are metabolized by cytochrome P450 enzymes, histamine does not induce their production. Histamine helps to maintain a wakeful state through an effect on Hj-receptors. Histamine-mediated hronchoconstriction is mediated by Hj-receptors, while histamine-mediated vasodilation occurs as a result of stimulation of Hi- and Hj-receptors. 

Mecftanism of Action AGI Hj-blocker and gastric acid secretion inhibitor that inhibits histamine action at histamine 2 receptors of parietal cells Therapeutic Effect Inhibits gastric acid secretion when fasting, at night, or when stimulated by food, caffeine, or insulin. 

Hormonal gastrin secreted by the G cells of the gastric antrum stimulates the parietal cells directly through gastrin receptors (increased Ca2+ as second messenger), and probably also indirectly by acting on enterochromaffin-iike (ECL) cells to release histamine. 

Histamine has long been recognized as a powerful stimulant of gastric acid secretion and, to a lesser extent, of gastric pepsin and intrinsic factor production. The effect is caused by activation of H2 receptors on gastric parietal cells and is associated with increased adenylyl... 

In close proximity to the parietal cells are gut endocrine cells called enterochromaffin-like (ECL) cells. ECL cells also have receptors for gastrin and acetylcholine, which stimulate histamine release. Histamine binds to the H2 receptor on the parietal cell, resulting in activation of adenylyl cyclase, which increases intracellular cyclic adenosine... 

Misoprostol has both acid inhibitory and mucosal protective properties. It is believed to stimulate mucus and bicarbonate secretion and enhance mucosal blood flow. In addition, it binds to a prostaglandin receptor on parietal cells, reducing histamine-stimulated cAMP production and causing modest acid inhibition. Prostaglandins have a variety of other actions, including stimulation of intestinal electrolyte and fluid secretion, intestinal motility, and uterine contractions. 

Inhibit basal and nocturnal gastric secretions by competitively and reversibly inhibiting the action of histamine at the histamine H -receptors of parietal cells... 

Figure 3. Effect of N -methylhistamine produced by Helicobacter pylori on acid secretion On the one hand, this compound may reduce acid secretion by inhibiting, via H3 receptor activation, histamine synthesis and release from ECL cells on the other hand, FI3 receptor activation on D cells, with consequent inhibition of somatostatin release, may increase acid secretion. Additionally, direct activation of H2 receptors on parietal cell by N -metylhistamine must also be considered (this mechanism is not shown in the scheme).

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