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Biomolecular Transport Dynamics Laboratory, Department of Chemical Engineering and the Bioengineering Program, The Pennsylvania State University, University Park, Pennsylvania 16802-4400
Significant changes in transvascular pressure occur in pulmonary hypertension, microgravity, and many other physiological and pathophysiological circumstances. Using bovine aortic endothelial cells grown on porous, rigid supports, we demonstrate that step changes in transmural pressure of 10, 20, and 30 cmH2O induce significant elevations in endothelial hydraulic conductivity (Lp) that require 5 h to reach new steady-state levels. The increases in Lp can be reversed by addition of a stable cAMP analog (dibutyryl cAMP), and the increases in Lp in response to pressure can be inhibited significantly with nitric oxide synthase inhibitors (NG-monomethyl-L-arginine and nitro-L-arginine methyl ester). The increase in Lp was not due to pressure-induced stretch because the endothelial cell (EC) support was rigid. It is unlikely that the increase in Lp was due to a direct effect of pressure because exposure of the cells to elevated pressure (25 cmH2O) for 4 h had no effect on the volume flux driven by a transmural pressure of 10 cmH2O. We hypothesize that elevated endothelial cleft shear stress induced by elevated transmural flow in response to elevated pressure stimulates the increase in Lp through a nitric oxide-cAMP-dependent mechanism. This is consistent with recent studies of the effects of shear stress on the luminal surface of ECs. We provide simple estimates of endothelial cleft shear stress, which suggest magnitudes comparable to those imposed by blood flow on the luminal surface of ECs.
endothelial cells; transmural pressure; nitric oxide; adenosine 3',5'-cyclic monophosphate
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