ARGININE VASOPRESSIN AND ATRIAL-NATRIURETIC-PEPTIDE DO NOT ALTER ION-TRANSPORT BY CULTURED FETAL DISTAL LUNG EPITHELIUM

Previous studies have shown that i.v. arginine vasopressin (AVP) decre ases but does not stop lung fluid secretion in term fetuses not in lab or. Although it has been presumed that the response to AVP results fro m augmented sodium transport, there is controversy whether AVP actuall y does affect sodium transport in mammalian lung epithelium. To determ ine if AVP or aldosterone could alone or together augment sodium trans port in the perinatal lung, we studied primary cultures of fetal rat d istal lung epithelium in Ussing chambers. The short circuit current of these sodium-transporting cells was not affected by the application o f either 30 or 300 mU/mL AVP whether or not they were previously expos ed to aldosterone (10(-6) M). Aldosterone also did not affect the base line bioelectric properties. Short circuit current increased in respon se to 8-bromo cAMP (10(-4) M) and +/- 3-isobutyl-1-methylxanthine (10( -3) M) to levels 169 +/- 16 (SEM) and 172 +/- 7% of respective baselin e values. AVP had no effect in cells pretreated with 3-isobutyl-1-meth ylxanthine. Monolayers also did not respond to atrial natriuretic pept ide (10(-11) to 10(-8) M). Monolayers of Na-absorbing A6 renal epithel ium did increase short circuit current with either aldosterone or AVP. AVP increased endogenous cAMP levels in A6 but not fetal rat distal l ung epithelium cells, suggesting that fetal rat distal lung epithelium lacks V2 receptors. These studies demonstrate that AVP does not incre ase ion transport in cultured fetal distal lung epithelium although th ese cells possess the necessary second messenger system.