title: Hydraulic conductance of pulmonary microvascular and macrovascular endothelial cell monolayers.
abstract: Endothelial cells isolated from pulmonary arteries (RPAEC) and microcirculation (RPMVEC) of rat lungs were grown to confluence on porous filters and mounted on an Ussing-type chamber. Transmembrane pressure (deltaP) was controlled by the reservoir height, and the filtration rate corrected for surface area (J(v)/A) was measured by timing fluid movement in a calibrated micropipette. These parameters were used to calculate hydraulic conductance (Lp) by using linear regression of J(v)/A on deltaP. Mean Lp values for newly confluent RPAEC monolayers were 22 times higher than those for RPMVEC monolayers (28.6 +/- 5.6 vs. 1.30 +/- 0.50 x 10(-7) cm x s(-1) x cmH2O(-1); P < or = 0.01). After confluence was reached, electrical resistance and Lp remained stable in RPAEC but continued to change in RPMVEC with days in culture. Both phenotypes exhibited an initial time-dependent sealing response, but Lp also had an inverse relationship to deltaP in RPMVEC monolayers > or = 4 days postconfluence that was attributed to cell overgrowth rather than junctional length. In a comparison of the cadherin contents, E-cadherin was predominant in RPMVEC, but VE-cadherin was predominant in RPAEC. At a constant deltaP of 40-45 cmH2O for 2 h, J(v)/A increased 225% in RPAEC monolayers but did not change significantly in RPMVEC monolayers. Significant decreases in Lp were obtained after treatment with 5% albumin, GdCl3, or isoproterenol plus rolipram in both phenotypes. Thus lung microvascular endothelial cells exhibited a significantly lower Lp than conduit vessel endothelium, which would limit alveolar flooding relative to perivascular edema cuff formation during increased pulmonary vascular pressures.
authors.affiliation: Dept. of Physiology, MSB 3074, College of Medicine, Univ. of South Alabama, Mobile, AL 36688, USA. Jparker@usouthal.edu
authors.forename: James C
authors.initials: JC
authors.lastname: Parker
authors.forename: Troy
authors.initials: T
authors.lastname: Stevens
authors.forename: Jason
authors.initials: J
authors.lastname: Randall
authors.forename: David S
authors.initials: DS
authors.lastname: Weber
authors.forename: Judy A
authors.initials: JA
authors.lastname: King
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000418:Albumins / Q000494:pharmacology; D000818:Animals; D015703:Antigens, CD; D015820:Cadherins / Q000378:metabolism; D002199:Capillary Permeability / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000378:metabolism* / Q000648:ultrastructure; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism*; D005374:Filtration; D005682:Gadolinium / Q000494:pharmacology; D017629:Gap Junctions / Q000378:metabolism / Q000648:ultrastructure; D007545:Isoproterenol / Q000494:pharmacology; D008168:Lung / Q000098:blood supply*; D008854:Microscopy, Electron; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D011312:Pressure; D011654:Pulmonary Edema / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020889:Rolipram / Q000494:pharmacology; D000099152:Cadherin 5
chemical_list: D000318:Adrenergic beta-Agonists; D000418:Albumins; D015703:Antigens, CD; D015820:Cadherins; D005682:Gadolinium; D007545:Isoproterenol; D010726:Phosphodiesterase Inhibitors; D020889:Rolipram; D000099152:Cadherin 5