of adenosine receptors known as A1, A2A, A2B, and A3. The A2B subtype is a low affinity receptor, which couples to stimulation of adenylyl cyclase and also leads to a rise in intracellular calcium modulating important physiol. processes. Adenosine exhibiting activity at this subtype is at concns. greater than 10 M. The A2B receptors show a ubiquitous distributions, the highest levels are present in cecum, colon and bladder, followed by blood vessels, mast cells and lung. Through A2B receptors, adenosine also regulates the growth of smooth muscle cell populations in blood vessels, cell growth, intestinal function, inhibition of Tumor Necrosis Factor (TNF-), vascular tone, and inflammatory processes such as diarrhea and asthma. Potent and selective adenosine agonists are the result of modifications of the parent ligand adenosine by substitution, namely at N6 or C2 position of the purine heterocycle or at the 5' position of the ribose moiety. 5'-N-ethylcarboxamidoadenosina (NECA) is one of the most potent A2B adenosine receptor agonist. Classical antagonists for A2B adenosine receptors are xanthine analogs obtained from multiple substitutions of the parent heterocycle by C8 substitution combined with N1 and N3 (and sometimes N7) substitutions.
Ligands for A(2B) adenosine receptor subtype
BARALDI, Pier Giovanni;ROMAGNOLI, Romeo;PRETI, Delia;FRUTTAROLO, Francesca;AGHAZADEH TABRIZI, Mojgan
2006
Abstract
of adenosine receptors known as A1, A2A, A2B, and A3. The A2B subtype is a low affinity receptor, which couples to stimulation of adenylyl cyclase and also leads to a rise in intracellular calcium modulating important physiol. processes. Adenosine exhibiting activity at this subtype is at concns. greater than 10 M. The A2B receptors show a ubiquitous distributions, the highest levels are present in cecum, colon and bladder, followed by blood vessels, mast cells and lung. Through A2B receptors, adenosine also regulates the growth of smooth muscle cell populations in blood vessels, cell growth, intestinal function, inhibition of Tumor Necrosis Factor (TNF-), vascular tone, and inflammatory processes such as diarrhea and asthma. Potent and selective adenosine agonists are the result of modifications of the parent ligand adenosine by substitution, namely at N6 or C2 position of the purine heterocycle or at the 5' position of the ribose moiety. 5'-N-ethylcarboxamidoadenosina (NECA) is one of the most potent A2B adenosine receptor agonist. Classical antagonists for A2B adenosine receptors are xanthine analogs obtained from multiple substitutions of the parent heterocycle by C8 substitution combined with N1 and N3 (and sometimes N7) substitutions.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
