Info

Results=means┬▒standard error *P<0.05 compared with controls

Control

120'

180'

Control

120'

180'

FIGURE 2-16 (Continued)

C, Urine flow rate and urinary sodium excretion over time. Inhibition of nitric oxide synthesis from L-arginine by a competitive substrate such as L-NAME produces dose-dependent and widespread vasoconstriction, leading to an increase in blood pressure [13]. Within specific regional beds such as the kidney, inhibition of nitric oxide produces a decrease in renal plasma flow, diminished glomerular filtration, and sodium retention [14]. The magnitude of these changes in normal animals and humans suggests that tonic nitric oxide production is a major endothelial buffering mechanism preserving vascular tone. The degree to which renal parenchymal disease alters the production of nitric oxide is not known precisely. In some situations, such as nephrotoxicity associated with cyclosporine administration, endothelial production of nitric oxide appears to be substantially impaired [15]. (Panel A from Rees and coworkers [13]; with permission. Panel B from Lahera and coworkers [14]; with permission.)

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