By John L. Wallace (auth.), Timothy S. Gaginella, Antonio Guglietta (eds.)
Drug improvement: Molecular pursuits for Gastrointestinal affliction brings jointly a panel of exotic specialists to significantly assessment the various promising new components of gastrointestinal pharmacology on the molecular point. Key chapters speak about such significant subject matters because the cyclooxygenase-2 inhibitors, the complexities of nitric oxide pathways within the intestine, and the impact of cytokines on inflammatory bowel sickness, in addition to new possibilities for pharmacotherapy, together with peptide development components, tachykinins-particularly substance P and neurokinins-cholecystokinin receptors, and serotonin. additionally tested as attainable websites for treating motility problems and visceral ache are the opioid receptors dwelling within the intestine, and the H3-receptor agonists for treating intestine irritation and ache. Drug improvement: Molecular objectives for Gastrointestinal sickness presents a accomplished overview of latest molecular pharmacological ways to the invention and improvement of novel medications for gastrointestinal and liver illnesses. Its huge references, richly skilled participants, and state-of-the-art syntheses of prior, current, and emergent examine identify the e-book as an important source for all pharmacologists, medicinal chemists, and clinicians looking extra strong medications for the prevention and remedy of gastrointestinal problems.
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Extra resources for Drug Development: Molecular Targets for GI Diseases
Sample text
Pylori infection. The control of such tissue damage with selective iNOS inhibitors may provide a complementary approach to peptic ulcer therapy. The involvement ofNO in the tissue injury associated with infectious diseases of the gut have also been explored. , 1996). , 1997). , 1997). , 1995). This slowly developing enteropathy involves indigenous bacteria, and is attenuated by inhibition of iNOS, Chapter 2 / NO Pathway in GI Disease 43 suggesting that, folIowing ingress of bacteria, lipopolysaccharide is liberated in the intestinal mucosa, which brings about the induction of iNOS.
1995). 4. , 1994; Shirgi-Degen and Beubler, 1995). Luminal administration of L-arginine Of the NO donor, SNAP, caused significant increases in water and electrolyte absorption. Furthermore, a NO donor attenuated the ileal secretion and permeability changes induced in rats by administration of C. , 1996). Similarly, sodium nitroprusside treatment was shown to inhibit jejunal secretion Chapter 2 / NO Pathway in GI Disease 33 in animals treated with Escherichia coli enterotoxin (Shirgi-Degen and Beubler, 1995).
Indeed, the therapeutic value of NO-containing NSAIDs is being actively pursued in experimental and clinical studies. The use of inhibitors of NO production is also being evaluated, especialIy as anti-inftammatory agents in the gut, but it is likely that NO produced from iNOS, or its subsequent products, are not involved in alI aspects of the inftammatory response in the gut. Because of their profile on leucocyte function, NO would not, for example, be expected to directly promote cellular infiltration.