[Modulated effects of prostaglandin E2 on endothelin production of alveolar macrophages in rats].
Using radioimmunoassay, we studied the endothelin (ET) production of alveolar macrophages(AM) of the rats. The results showed that: (1) a basal amount of ET which was time-dependent (r = 0.7415, P < 0.01) was detected in supernatant of cultured unstimulated AM; (2) lipopolysaccharide (LPS), PMA, or A23187 could increase the ET production of AM (P < 0.01) (3) calmodulin antagonist W7 reduced the ET production of LPS or A23187-stimulated AM (P < 0.05, P < 0.01), but did not effect that of PMA-stimulated AM; protein kinase C inhibitor H7 attenuated the effect of PMA on ET production (P < 0.01), but did not effect LPS on ET production; (4) prostaglandin E2 (PGE2) inhibited the ET production of LPS-stimulated (P < 0.05) and PMA-stimulated AM (P < 0.05); cyclooxygenase inhibitor indomethacin enhanced the effect of LPS on ET production (P < 0.01), but did not effect PMA on ET production. We conclude that AM is an important source of ET in the lungs both at physiologic and pathologic situation there are two pathways of signal transduction for factors stimulating ET production of AM, i.e., PKC-dependent and Ca(2+)-calmodulin-dependent pathways; the autocrine PGEs from AM shows a negatively modulated effect on ET production of AM.
Luo
Z
Z
Department of Physiology, Hunan Medical University, Changsha.
Sun
X
X
D000818:Animals; D015232:Dinoprostone / Q000494:pharmacology*; D016232:Endothelins / Q000096:biosynthesis*; D005260:Female; D016676:Macrophages, Alveolar / Q000378:metabolism*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction
D016232:Endothelins; D015232:Dinoprostone