Letter to the Editor |
Hannover Medical School, Institute of Clinical Pharmacology, Hannover, Germany, tsikas.dimitros@mh-hannover.de
To the Editor:
The discovery of the endothelium-derived relaxing factor (EDRF), its identification as nitric oxide (·NO), and the recognition of its multiple biological functions, especially in the cardiovascular system, are fascinating scientific achievements of the last two decades, an effort that was awarded the Nobel Prize for Medicine in 1998.
Curiously, no other small molecule like ·NO challenges so many scientists from so very different disciplines. In the literature, there is no further example for the development and application of so wide a spectrum of analytical approaches and methods in recent years that has yielded highly divergent values, often within a range of three orders of magnitude, and has consequently led to numerous deceptive conclusions.
In 1992, Stamler et al1 reported for the first time that ·NO circulates in plasma of healthy humans primarily as S-nitrosoalbumin (SNALB; 7000 nmol/L, n=5). Mainly on the basis of this finding, Stamlers group1 suggested that SNALB may be a physiological reservoir of ·NO, by which ·NO-related actions such as vasodilation are regulated in humans. This highly interesting finding has initiated much scientific work in this area.
Until today, however, there is no solid confirmation, perhaps with a single exception,2 of Stamlers originally reported values for endogenous normal plasma levels of SNALB, not even by Stamler himself, who communicated3 in 1997 that normal SNALB plasma levels may be much lower, ie 200 to 1000 nmol/L.
In 1999, for the first time, we questioned4 Stamlers findings on endogenous normal SNALB plasma levels. By means of a
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D. Tsikas and J. C. Frolich Are plasma S-nitrosothiol levels elevated in chronic renal failure? Nephrol. Dial. Transplant., October 1, 2003; 18(10): 2199 - 2199. [Full Text] [PDF] |
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