[Modulation of endothelin-1 on pulmonary surfactant synthesis in lung explants].
The effect of endothelin-1(ET-1) on pulmonary surfactant(PS) synthesis was studied in cultured lung explants without serum. The results showed that: 1. ET-1 increased [3H] choline incorporation with dose-dependence and time-dependence. 10(-10) mol.L-1 ET-1 increased the contents of total phospholipids, phosphatidylcholine and phosphatidylglcerol in lung tissues. The major membrane characteristic phospholipids, such as phosphatidylethanolamine, phosphatidylinostitol, phosphatidylserine and sphingomyelin, did not show changes. 2. BQ123, a ETA receptor selective antagonist, could decline the [3H] choline incorporation induced by ET-1(10(-12) and 10(-10) mol.L-1) (P < 0.01). 3. PMA, a protein kinase C(PKC) activator, increased [3H] choline incorporation into lung tissues (P < 0.01); the PKC inhibitor H7 decreased [3H] choline incorporation induced by ET-1(P < 0.01). The results demonstrated that ET-1 at physiological level can enhance the PS synthesis mediated by ETA receptor and PKC.
Luo
Z
Z
Department of Physiology, Hunan Medical University, Changsha.
Sun
X
X
Qing
X
X
D000818:Animals; D046508:Culture Techniques; D019332:Endothelin-1 / Q000494:pharmacology*; D005260:Female; D008168:Lung / Q000378:metabolism*; D008297:Male; D011493:Protein Kinase C / Q000494:pharmacology; D011663:Pulmonary Surfactants / Q000096:biosynthesis*; D051381:Rats; D017208:Rats, Wistar; D017466:Receptors, Endothelin / Q000378:metabolism
D019332:Endothelin-1; D011663:Pulmonary Surfactants; D017466:Receptors, Endothelin; D011493:Protein Kinase C