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ACTIONS OF NITRIC OXIDE ON RENAL EPITHELIAL TRANSPORT
Author(s) -
Stoos BA,
Garvin JL
Publication year - 1997
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1997.tb02097.x
Subject(s) - natriuresis , nitric oxide , chemistry , endocrinology , medicine , in vivo , sodium , proximal tubule , nephron , perfusion , kidney , biophysics , biology , microbiology and biotechnology , organic chemistry
SUMMARY 1. In vivo studies have demonstrated that nitric oxide (NO) induces natriuresis. Nitric oxide‐induced natriuresis occurs independently of changes in renal perfusion pressure, indicating that it is the result of a tubular effect of NO. 2. In support of this hypothesis investigators have shown that NO inhibits both Na + ‐H + exchange and Na + /K + ‐ATPase activity in the proximal tubule. In the collecting duct, NO has been shown to decrease sodium flux with no effect on Na + /K + ‐ATPase activity. 3. Thus, direct examination of the actions of NO have shown that NO can inhibit sodium transport in the nephron, which may account for the natriuresis observed in vivo.