Opposing effects of L-NAME on capillary filtration rate in the presence or absence of neutrophils.

Abstract

Fluid filtration rate (JV/S) from rat mesenteric capillaries was measured using a modified Landis technique before and after superfusion with 100 microM NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor. Three groups were studied: 1) control rats, 2) rats injected with antineutrophil serum (ANS), and 3) rats injected with a monoclonal antibody (CL26) against the leukocyte adhesion molecule CD18. The relative increase in JV/S (L-NAME/ baseline) in control rats averaged 1.66 +/- 0.32 (n = 11), which was significantly higher (P < 0.05) than in ANS (0.51 +/- 0.12; n = 5)- and CL26 (0.45 +/- 0.16; n = 6)-injected rats exposed to L-NAME. The L-NAME-induced changes in JV/S in each group were due to altered permeability rather than altered pressure gradients, as determined by measurements of arteriolar hydrostatic pressure (using a servo-null apparatus) and estimates of intravascular oncotic pressure (using plasma protein concentration). These findings indicate that nitric oxide synthase inhibition increases the permeability of mesenteric capillaries to water, a response that is dependent on neutrophil adhesion.