Browsing Pathways

Dinoprost tromethamine is a prostaglandin E1 analog that reduces the risk of NSAID-induced gastric ulcers. Dinoprost tromethamine stimulates prostaglandin receptors on parietal cells in the stomach to reduce gastric acid secretion. Dinoprost tromethamine activates prostaglandin EP3 receptors in parietal cells. Activation of this receptor triggers the Gi protein signaling cascade, inhibiting adenylate cyclase. Adenylate cyclase is responsible for converting ATP to cAMP, therefore, inhibition of adenylate cyclase reduces cytosolic cAMP concentration. cAMP is responsible for activating protein kinase A. With lower concentrations of cAMP, less protein kinase A is activated. Protein kinase A activates the proton pump in the luminal membrane of the parietal cell. The role of the proton pump is to secrete acid (H+) into the stomach lumen. With reduced protein kinase A activation, this decreases the activity of the proton pump, fewer H+ ions are pumped into the lumen, reducing the acidity and thus allowing stomach ulcers to heal and reducing the pain caused by the ulcers. Dinoprost tromethamine may also promote ulcer healing by increasing mucus and bicarbonate secretion and thickening the mucosal bilayer so the mucosa can generate new cells.

Latanoprost is a prostaglandin E1 analog that reduces the risk of NSAID-induced gastric ulcers. Latanoprost stimulates prostaglandin receptors on parietal cells in the stomach to reduce gastric acid secretion. Latanoprost activates prostaglandin EP3 receptors in parietal cells. Activation of this receptor triggers the Gi protein signaling cascade, inhibiting adenylate cyclase. Adenylate cyclase is responsible for converting ATP to cAMP, therefore, inhibition of adenylate cyclase reduces cytosolic cAMP concentration. cAMP is responsible for activating protein kinase A. With lower concentrations of cAMP, less protein kinase A is activated. Protein kinase A activates the proton pump in the luminal membrane of the parietal cell. The role of the proton pump is to secrete acid (H+) into the stomach lumen. With reduced protein kinase A activation, this decreases the activity of the proton pump, fewer H+ ions are pumped into the lumen, reducing the acidity and thus allowing stomach ulcers to heal and reducing the pain caused by the ulcers. Latanoprost may also promote ulcer healing by increasing mucus and bicarbonate secretion and thickening the mucosal bilayer so the mucosa can generate new cells.

Travoprost is a prostaglandin E1 analog that reduces the risk of NSAID-induced gastric ulcers. Travoprost stimulates prostaglandin receptors on parietal cells in the stomach to reduce gastric acid secretion. Travoprost activates prostaglandin EP3 receptors in parietal cells. Activation of this receptor triggers the Gi protein signaling cascade, inhibiting adenylate cyclase. Adenylate cyclase is responsible for converting ATP to cAMP, therefore, inhibition of adenylate cyclase reduces cytosolic cAMP concentration. cAMP is responsible for activating protein kinase A. With lower concentrations of cAMP, less protein kinase A is activated. Protein kinase A activates the proton pump in the luminal membrane of the parietal cell. The role of the proton pump is to secrete acid (H+) into the stomach lumen. With reduced protein kinase A activation, this decreases the activity of the proton pump, fewer H+ ions are pumped into the lumen, reducing the acidity and thus allowing stomach ulcers to heal and reducing the pain caused by the ulcers. Travoprost may also promote ulcer healing by increasing mucus and bicarbonate secretion and thickening the mucosal bilayer so the mucosa can generate new cells.

Latanoprostene bunod is a prostaglandin E1 analog that reduces the risk of NSAID-induced gastric ulcers. Latanoprostene bunod stimulates prostaglandin receptors on parietal cells in the stomach to reduce gastric acid secretion. Latanoprostene bunod activates prostaglandin EP3 receptors in parietal cells. Activation of this receptor triggers the Gi protein signaling cascade, inhibiting adenylate cyclase. Adenylate cyclase is responsible for converting ATP to cAMP, therefore, inhibition of adenylate cyclase reduces cytosolic cAMP concentration. cAMP is responsible for activating protein kinase A. With lower concentrations of cAMP, less protein kinase A is activated. Protein kinase A activates the proton pump in the luminal membrane of the parietal cell. The role of the proton pump is to secrete acid (H+) into the stomach lumen. With reduced protein kinase A activation, this decreases the activity of the proton pump, fewer H+ ions are pumped into the lumen, reducing the acidity and thus allowing stomach ulcers to heal and reducing the pain caused by the ulcers. Latanoprostene bunod may also promote ulcer healing by increasing mucus and bicarbonate secretion and thickening the mucosal bilayer so the mucosa can generate new cells.

Tafluprost is a prostaglandin E1 analog that reduces the risk of NSAID-induced gastric ulcers. Tafluprost stimulates prostaglandin receptors on parietal cells in the stomach to reduce gastric acid secretion. Tafluprost activates prostaglandin EP3 receptors in parietal cells. Activation of this receptor triggers the Gi protein signaling cascade, inhibiting adenylate cyclase. Adenylate cyclase is responsible for converting ATP to cAMP, therefore, inhibition of adenylate cyclase reduces cytosolic cAMP concentration. cAMP is responsible for activating protein kinase A. With lower concentrations of cAMP, less protein kinase A is activated. Protein kinase A activates the proton pump in the luminal membrane of the parietal cell. The role of the proton pump is to secrete acid (H+) into the stomach lumen. With reduced protein kinase A activation, this decreases the activity of the proton pump, fewer H+ ions are pumped into the lumen, reducing the acidity and thus allowing stomach ulcers to heal and reducing the pain caused by the ulcers. Tafluprost may also promote ulcer healing by increasing mucus and bicarbonate secretion and thickening the mucosal bilayer so the mucosa can generate new cells.

The pharmacological activity of aripiprazole lauroxil is thought to be mainly mediated by its metabolite aripiprazole, and to a lesser extent, dehydro-aripiprazole. Aripiprazole functions as a partial agonist at the dopamine D2 and the serotonin 5-HT1A receptors, and as an antagonist at the serotonin 5-HT2A receptor

Aceprometazine is a is a drug with neuroleptic and anti-histamine properties. Although not widely prescribed, it is used in combination with meprobamate for the treatment of sleep disorders in France under the trade name Mepronizine. Aceprometazine, acting as an H1-receptor antagonist can induce sedation by being able to cross the blood-brain-barrier and binding to H1-receptors in the central nervous system. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. H1-antihistamines act on H1 receptors in T-cells to inhibit the immune response, in blood vessels to constrict dilated blood vessels, and in smooth muscles of lungs and intestines to relax those muscles. Allergies causes blood vessel dilation which causes swelling (edema) and fluid leakage.

Benzquinamide is a first-generation ethanolamine H1-antihistamine. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.