New PDF release: A3 Adenosine Receptors from Cell Biology to Pharmacology and

By John R. Fozard (auth.), Pier Andrea Borea (eds.)

ISBN-10: 904813143X

ISBN-13: 9789048131433

ISBN-10: 9048131448

ISBN-13: 9789048131440

This ebook "A3 Adenosine Receptors from phone Biology to Pharmacology and Therapeutics " records the current country of data of the adenosine A3 receptor. Adenosine A3 receptors are G protein-linked receptors that functionality in body structure and intracellular signaling and are focused on inflammatory responses and mediating cellphone proliferation and telephone loss of life.

The A3 receptor is more and more being well-known for its organic roles during the physique, and plenty of A3 receptor ligands have confirmed beneficial in elucidating peripheral and vital pathologies. This ebook covers quite a lot of info together with information from reports of theoretical, molecular and mobile pharmacology, sign transduction, integrative body structure, new drug discoveries and scientific functions. The ebook comprises sections on:

  • A3 Adenosine Receptor sign transduction
  • Adenosine Receptor medicinal chemistry
  • Effects and healing functions of Adenosine Receptors on tissues and organs
  • Adenosine Receptors and inflammatory and auto-immune diseases
  • Adenosine Receptors and cancer

The chapters during this publication hide either basic technology and appropriate purposes and supply an authoritative account of the present prestige of the sphere. "A3 Adenosine Receptors from cellphone Biology to Pharmacology and Therapeutics" is an up to the moment and scientifically first-class resource of knowledge, beautiful to easy and medical scientists alike.

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Additional resources for A3 Adenosine Receptors from Cell Biology to Pharmacology and Therapeutics

Sample text

8). R. 3 mg kg−1 intratracheally). Responses are expressed relative to the response to bethanechol (100 mM) which was taken as 100%. Mean values (± SEM) from the number of individual experiments shown in parentheses are presented. 7) it can be concluded that 2-Cl-IB-MECA and methysergide act on the same component in the response to adenosine which is mast cell mediated. Moreover, selective blockade of adenosine by 2-Cl-IB-MECA at low concentrations would be consistent with the A3 receptor being involved in the response.

In the case of NECA, the concentrations ranged between 3 and 100 mM which are respectively 10–300 times the Ki value at the rat A3 receptor and 400–14,000 times the Ki value at the A1 receptor (Fredholm et al. 2001a). On this basis, we decided to re-evaluate the effects of CPA and 2-Cl-IB-MECA at concentrations higher than those used previously. 6). 5). 3 mg kg−1; filled columns) or saline (open columns). Responses are expressed relative to the response to bethanechol (100 mM) which was taken as 100%.

As a consequence a high degree of correlation between intrinsic activity and DS° values was reported for adenosine ligands acting as full or partial agonists and as antagonists (Borea et al. 1994). 3b). As for the glycine receptor, the agonist binding has to be classified as entropy-driven (2 £ DH° £ 20 kJ/mol; −56 £ −TDS° £ −25 kJ/mol), whereas the antagonist binding is mostly enthalpy-driven (−58 £ DH° £ −15 kJ/mol; −15 £ −TDS° £ 29 kJ/mol) (Gomez et al. 1989). Agonist binding to the GABAA receptor is entropy-driven (−1 £ DH° £ 14 kJ/mol; −48 £ −TDS° £ −28 kJ/mol) while antagonist binding is enthalpy- and entropy-driven (−23 £ DH° £ −12 kJ/mol; −31 £ −TDS° £ −15 kJ/mol) (Maksai 1994).

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A3 Adenosine Receptors from Cell Biology to Pharmacology and Therapeutics by John R. Fozard (auth.), Pier Andrea Borea (eds.)

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