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Am J Physiol Heart Circ Physiol 279: H2017-H2023, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 4, H2017-H2023, October 2000

RAPID COMMUNICATION
Differential effects of L-NAME on rat venular hydraulic conductivity

Rolando E. Rumbaut, Jianjie Wang, and Virginia H. Huxley

Pulmonary and Critical Care Division, Department of Internal Medicine, and Department of Physiology, University of Missouri-Columbia, Columbia, Missouri 65212

The role of nitric oxide (NO) in microvascular permeability remains unclear because both increases and decreases in permeability by NO synthase (NOS) inhibitors have been reported. We sought to determine whether blood-borne constituents modify venular permeability responses to the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME). We assessed hydraulic conductivity (Lp) of pipette-perfused rat mesenteric venules before and after exposure to 10-4 M L-NAME. In the absence of blood-borne constituents, L-NAME reduced Lp by nearly 50% (from a median of 2.4 × 10-7 cm · s-1 · cmH2O-1, n = 17, P < 0.001). The reduction in Lp by L-NAME was inhibited by a 10-fold molar excess of L-arginine but not D-arginine (n = 6). In a separate group of venules, blood flow was allowed to resume during exposure to L-NAME. In vessels perfused by blood during L-NAME exposure, Lp increased by 78% (from 1.4 × 10-7 cm · s-1 · cmH2O-1, n = 10, P < 0.01). NG-nitro-D-arginine methyl ester did not affect Lp in either of the two groups. These data imply that NO has direct vascular effects on permeability that are opposed by secondary changes in permeability mediated by blood-borne constituents.

microvascular permeability; arginine; endothelium; rat; nitric oxide synthase


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