Comparison of regulatory action of cAMP and cGMP on the activation of neutrophil responses.
- Author:
Chang Hwang HAN
1
;
Young Chul YOON
;
Yong Kyoo SHIN
;
Eun Sook HAN
;
Chung Soo LEE
Author Information
1. Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul 156-756 South Korea.
- Publication Type:Original Article
- MeSH:
Adenosine;
Bucladesine;
Calmodulin;
Chlorpromazine;
Genistein;
Hand;
Histamine;
Neutrophils*;
Nitroprusside;
Nucleotides, Cyclic;
Protein Kinase C;
Protein-Tyrosine Kinases;
Staurosporine;
Superoxides;
Theophylline
- From:The Korean Journal of Physiology and Pharmacology
1997;1(1):97-105
- CountryRepublic of Korea
- Language:English
-
Abstract:
The regulatory role of cyclic nucleotides in the expression of neutrophil responses has been examined. fMLP-stimulated superoxide production in neutrophils was inhibited by dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), histamine, adenosine + theophylline, cAMP elevating agents, and 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP) and sodium nitroprusside, cGMP elevating agents. Staurosporine, a protein kinase C inhibitor, genistein, a protein tyrosine kinase inhibitor and chlorpromazine, a calmodulin inhibitor, inhibited superoxide production by fMLP, but they did not further affect the action of DBcAMP on the stimulatory action of fMLP. DBcAMP, histamine, adenosine + theophylline and genistein inhibited myeloperoxidease release evoked by fMLP, whereas BrcGMP, sodium nitroprusside and staurosporine did not affect it. The elevation of (Ca2+)-i evoked by fMLP was inhibited by genistein and chlorpromazine but was not affected by staurosporine. DBcAMP exerted little effect on the initial peak in (Ca2+)-i response to fMLP but effectively inhibited the sustained rise. On the other hand, BrcGMP significantly inhibited both phases. fMLP-induced Mn-2+ influx was inhibited by either DBcAMP or BrcGMP. These results suggest that fMLP-stimulated neutrophil responses may be regulated by cAMP more than cGMP. cAMP and cGMP appear not affect stimulated responses by direct protein kinase C activation. Their regulatory action on the stimulated neutrophil responses may be not influenced by other activation processes.
