Article date: October 1994
By: Helen Wise, Robert L. Jones, in Volume 113, Issue 2, pages 581-587
The effects of various prostanoid agonists have been compared on the increase in intracellular free calcium ([Ca2+]i) and the aggregation reaction of rat peritoneal neutrophils induced by N‐formyl‐L‐methionyl‐L‐leucyl‐L‐phenylalanine (FMLP).
Prostaglandin E2 (PGE2) and the specific IP‐receptor agonist, cicaprost, both inhibited the FMLP‐induced increase in [Ca2+]i (IC50 33 nm and 18 nm respectively) and the FMLP‐induced aggregation reaction (IC50 5.6 nm and 7.9 nm respectively). PGD2, PGF2α, and the TP‐receptor agonist, U 46619, were inactive at the highest concentration tested (1 μm).
The EP1receptor agonist, 17‐phenyl‐ω‐trinor PGE2, and the EP3‐receptor agonists, GR 63799X and sulprostone, had no inhibitory effect on FMLP‐stimulated rat neutrophils.
PGE1 (EP/IP‐receptor agonist) and iloprost (IP‐receptor agonist) inhibited the FMLP‐induced increase in [Ca2+]i with IC50 values of 34 nm and 38 nm respectively. The EP2‐receptor agonists, butaprost and misoprostol (1 μm), inhibited both FMLP‐stimulated [Ca2+]i and aggregation. However another EP2‐receptor agonist, AH 13205, was inactive in both assays.
Prostanoid receptors present on rat neutrophils were further characterized by measuring [3H]‐adenosine 3′:5′‐cyclic monophosphate ([3H]‐cyclic AMP) accumulation. Only those agonists capable of stimulating [3H]‐cyclic AMP accumulation were able to inhibit both FMLP‐stimulated [Ca2+]i and aggregation.
These results indicate that rat neutrophils possess inhibitory IP and EP‐receptors; the relative potencies of PGE2, misoprostol and butaprost are those expected for the EP2‐receptor subtype. No evidence for DP, FP, TP or EP1 and EP3‐receptors was obtained.
The effects of various prostanoid agonists have been compared on the increase in intracellular free calcium ([Ca2+]i) and the aggregation reaction of rat peritoneal neutrophils induced by N‐formyl‐L‐methionyl‐L‐leucyl‐L‐phenylalanine (FMLP).
Prostaglandin E2 (PGE2) and the specific IP‐receptor agonist, cicaprost, both inhibited the FMLP‐induced increase in [Ca2+]i (IC50 33 nm and 18 nm respectively) and the FMLP‐induced aggregation reaction (IC50 5.6 nm and 7.9 nm respectively). PGD2, PGF2α, and the TP‐receptor agonist, U 46619, were inactive at the highest concentration tested (1 μm).
The EP1receptor agonist, 17‐phenyl‐ω‐trinor PGE2, and the EP3‐receptor agonists, GR 63799X and sulprostone, had no inhibitory effect on FMLP‐stimulated rat neutrophils.
PGE1 (EP/IP‐receptor agonist) and iloprost (IP‐receptor agonist) inhibited the FMLP‐induced increase in [Ca2+]i with IC50 values of 34 nm and 38 nm respectively. The EP2‐receptor agonists, butaprost and misoprostol (1 μm), inhibited both FMLP‐stimulated [Ca2+]i and aggregation. However another EP2‐receptor agonist, AH 13205, was inactive in both assays.
Prostanoid receptors present on rat neutrophils were further characterized by measuring [3H]‐adenosine 3′:5′‐cyclic monophosphate ([3H]‐cyclic AMP) accumulation. Only those agonists capable of stimulating [3H]‐cyclic AMP accumulation were able to inhibit both FMLP‐stimulated [Ca2+]i and aggregation.
These results indicate that rat neutrophils possess inhibitory IP and EP‐receptors; the relative potencies of PGE2, misoprostol and butaprost are those expected for the EP2‐receptor subtype. No evidence for DP, FP, TP or EP1 and EP3‐receptors was obtained.
DOI: 10.1111/j.1476-5381.1994.tb17029.x
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