Histamine receptors inhibitors effects

In another example of a hybrid DDS, ranitidine hydrochloride, the H2 histamine receptor inhibitor, was intercalated in MMT and coated with the cationic polymer Eudragit ElOO using an oil-in-water solvent evaporation method. The material obtained had the form of microparticles. It vras found that in the presence of Eudragit ElOO, both the release rate and the amount of drug released noticeably increased, because of the effective exchange of the polycation with intercalated drug molecules. In a similar... 

With the introduction of the SSRIs, the safety and tolerability of antidepressants improved remarkably. As a class, these medications have little or no affinity for cholinergic, (3-adrenergic or histamine receptors and do not interfere with cardiac conduction. They are well tolerated by patients with heart disease and by the elderly, who are especially sensitive to the anticholinergic and orthostatic effects of the tricyclic antidepressant agents (TCAs) and monoamine oxidase inhibitors (MAOIs). 

The effects of histamine on body tissues and organs can be diminished in four ways inhibition of histamine synthesis, inhibition of histamine release from storage granules, blockade of histamine receptors, and physiological antagonism of histamine s effects. Of these approaches, only the inhibition of histamine synthesis has not been employed clinically. The focus of this chapter is on Hi histamine receptor antagonists it provides a brief overview of the H2 blockers and the inhibitors of histamine release. More details can be found in Chapters 39 and 40. 

Several nonsedative Hj inhibitors have been marketed—for example, astemizole (4.149) and terfenadine (4.150). They are quite polar molecules and therefore cannot cross the blood-brain barrier to reach central histamine receptors. This is a good example of drug design exploiting knowledge of the pharmacokinetic processes to preclude undesirable CNS side effects. 

Imipramine Mixed and variable blockade of NET and SERT Like SNRIs plus significant blockade of autonomic nervous system and histamine receptors Major depression not responsive to other drugs chronic pain disorders incontinence obsessive-compulsive disorder (clomipramine) Long half-lives CYP substrates active metabolites Toxicity Anticholinergic, G.-blocking effects, sedation, weight gain, arrhythmias, and seizures in overdose Interactions CYP inducers and inhibitors... 

The adverse effects profile of the proton pump inhibitors during short-term administration (under 12 weeks) is similar to that reported with short-term use of histamine receptor antagonists. The type and frequency of adverse effects reported with lansoprazole, omeprazole, pantoprazole, and rabeprazole are comparable. The most common adverse effects include headache, diarrhea, nausea, abdominal pain, constipation, dizziness, and skin rashes. 

V. cholerae is a gram-negative baciUus sharing similar characteristics with the family Enterobacteriaceae. Most pathology of cholera results from an enterotoxin (cholera toxin) produced by the bacteria. Conditions that reduce gastric acidity, such as the use of antacids, histamine-receptor blockers, or proton pump inhibitors or infections with Helicobacter pylori, increase the risk for clinical disease. Cholera toxin stimulates adenylate cyclase, which increases intracellular cAMP and results in inhibition of sodium and chloride absorption by microvillli and promotes the secretion of chloride and water by crypt cells. The toxin likely acts along the entire intestinal tract, but most fluid loss occurs in the duodenum. The net effect of the cholera toxin is isotonic fluid secretion (primarily in the small intestine) that exceeds the absorptive capacity of the intestinal tract (primarily the colon). This results in the production of watery diarrhea with electrolyte concentrations similar to that of plasma. 

Multiple stimuli for the release of gastric acid exist, so blockade of the histamine receptor only decreases secretion to the extent that other stimuli are present or absent. Proton-pump inhibitors act at the last step of gastric acid synthesis and thus are not subject to the effects of other mediators. 

Although it does not act at any histamine receptor, epinephrine reverses many effects of histamine. Epinephrine is a (A) Competitive inhibitor of histamine... 

As we move forward with our discussion, we ll devote a section of this chapter to each of the key neurotransmitter systems that psychotropic medications interact with. We will discuss the following systems norepinephrine, dopamine, serotonin, GABA, acetylcholine, and histamine. Within each of the sections is a description of the effects that can be anticipated when a medication enhances the activity of that transmitter (reuptake inhibitors or agonists), and the effects to expect when a medication interferes (receptor antagonists) with the activity of that same transmitter. We will then describe strategies that can be implemented to help minimize and/or manage these side effects. 

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. 

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. 

Venlafaxine is a serotonin and noradrenaline reuptake inhibitor (SNRI). It shares these properties with the TCAs amitriptyhne, clomipramine and imip-ramine, but it is the first selective SNRI, with low affinity for muscarinic, histaminic and a-adrenergic receptors. At low doses serotonergic effects predominate, but at higher doses the reuptake of noradrenaline is significantly blocked (Melichar et al. 2001). It is available as immediate and extended release (XR) preparations. 

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. 

Although the SSRIs provided a tremendous advantage over the TCAs in terms of tolerability, an effect on norepinephrine also has some theoretical advantages. For example, some authors have suggested that dual reuptake inhibitors may be more likely to lead to remission (Thase et al. 2001). As the name of the class implies, these agents affect the reuptake of both serotonin and norepinephrine, while having very little effect on muscarinic, histaminic or Hj, or aj-adrenergic receptors. Hence these medications share many of the tolerability and safety benefits of the SSRIs. Currently, two serotonin-norepinephrine reuptake inhibitors (SNRIs) are available in the United States venlafaxine and duloxetine. 

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