English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Sohji Nagase, MD, PhD, Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Ten-nodai, Tsukuba, Ibaraki 305 (Japan), Tel/Fax +81 (298) 53-3202, E-Mail sohji-n@md.tsukuba.ac.jp Dear Sir, We read with great interest the report by Dr. Rivas-Cabañero et al. [1] published as a letter to the editor in Nephron last year. The authors found that nitrite and nitrate, stable oxidative products of NO (N02 + N03 = NOx) actually increase during the administration of the nitric oxide synthase (NOS) inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), in the longterm incubation of isolated glomeruli. In fact, the concentration of NOx in the incubation medium containing L-NAME is higher than that of controls after 8 h of incubation. The Griess reaction was employed to measure NOx in the study. The authors speculated that the stimulated NO production is derived from enzymatic synthesis of L-arginine from L-NAME. On the other hand, a recent publication by Dr. Heyman et al. [2] demonstrates, using a Clarktype electrode to measure NO, a paradoxical increase in renal medullary NO production. These authors report that outer medullary NO electrode current did not fall but rose following the addition of L-NAME to renal perfusate despite a rise in blood pressure. They hypothesized that the NO current may reciprocally increase during a reduction in tissue oxygenation, as less NO is being scavenged by oxygen and reactive oxygen species. The possibility of a renal substance that interferes with the electrode current has also been considered. Recently, we reported that NOx, detected by the Griess reaction, increases following the reaction of hydrogen peroxide and D-arginine, L-arginine, L-canavanine, or even L-NAME. However, when we used chemilu-minescence for the detection of NO, it was detected only from the reactions of hydrogen peroxide and Dor L-arginine. We conclude that there is a pathway for NO synthesis from Dand L-arginine not dependent upon the action of NOS and that the use of NOx as a marker of NO generation is unreliable because nitrite and/or nitrate rather than NO could be released from L-canavanine and L-NAME through the action of hydrogen peroxide [3]. In addition, in a study monitoring NO generation by Clark-type electrode, we found that the existence of hydrogen peroxide alone

nephron

NO Is Not Exclusively Generated by the Reaction of &lt;i&gt;L&lt;/i&gt;-Arginine and NOS and Is Poorly Identified by the Griess Reaction or Clark-Type Electrodes