Enhanced nitric oxide synthesis in uremia: Implications for platelet dysfunction and dialysis hypotension

Marina Noris, Ariela Benigni, Paola Boccardo, Sistiana Aiello, Flavio Gaspari, Marta Todeschini, Marina Figliuzzi, Giuseppe Remuzzi

Research output: Contribution to journalArticlepeer-review

Abstract

Nitric oxide (NO), a potent vasodilator which also inhibits platelet adhesion and aggregation, is generated by endothelial cells and platelets from its precursor L-arginine. Since N-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthesis, normalizes the prolonged bleeding time of uremic rats, it has been suggested that bleeding associated with uremia was due to an excessive NO formation. With the present study we sought to evaluate whether in patients with chronic renal failure - like in uremic ratsdefective platelet aggregation were associated with excessive formation of NO and whether uremic plasma promotes NO synthesis by cultured vascular endothelium. Data indicated that plasma L-arginine was higher in uremics than in controls, uremic platelets generated more NO than control platelets, and intraplatelet levels of cGMP (the NO second messenger) were also higher in uremic than in control platelets. Moreover, uremic plasma potently induced NO synthesis by cultured endothelial cells, a phenomenon which was further amplified by adding to uremic plasma endotoxin and interferon γ. Increased NO biosynthesis may contribute to platelet dysfunction and possibly other manifestations of uremic syndrome, including hemodialysis hypotension.

Original languageEnglish
Pages (from-to)445-450
Number of pages6
JournalKidney International
Volume44
Issue number2
Publication statusPublished - Aug 1993

ASJC Scopus subject areas

  • Nephrology

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