Premium
Effects of adenosine on polymorphonuclear leucocyte function, cyclic 3′:5′‐adenosine monophosphate, and intracellular calcium
Author(s) -
Nielson Christopher P.,
Vestal Robert E.
Publication year - 1989
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1989.tb12028.x
Subject(s) - adenosine , calcium , calcium in biology , intracellular , chemistry , fura 2 , medicine , endocrinology , adenosine receptor , biochemistry , biology , receptor , agonist , enzyme , cytosol
1 Inhibition of human polymorphonuclear leucocyte (PMN) function by adenosine was studied with respect to effects of adenosine on intracellular cyclic AMP and calcium during the PMN respiratory burst. 2 The adenosine analogue 5′‐N‐ethylcarboxamide‐adenosine (NECA) and L‐N 6 ‐phenyl‐isopropyladenosine (L‐PIA) inhibited PMN oxygen metabolite generation with relative potencies (NECA > adenosine > L‐PIA) characteristic of an A 2 receptor. 3 The respiratory burst was inhibited by adenosine when PMN were activated by calcium ionophore or chemotactic peptide but not when cells where activated by oleoyl‐acetyl‐glycerol (OAG). 4 Adenosine increased intracellular cyclic AMP during the PMN respiratory burst regardless of whether cells were stimulated by ionophore, chemotactic peptide or OAG. 5 To determine whether the differences in cell inhibition by adenosine were related to differences in intracellular calcium mobilization by each activating agent, calcium was evaluated with the fluorescent probe, indo‐1. Adenosine suppressed the increase in intracellular calcium following PMN activation by calcium ionophore or chemotactic peptide. In contrast, calcium did not increase in PMN activated by OAG and adenosine did not affect intracellular calcium changes following this stimulus. 6 These results demonstrate that physiological concentrations of adenosine inhibit the PMN respiratory burst in association with an increase in intracellular cyclic AMP and reduction of intracellular calcium.