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Interactions between nitric oxide and prostanoids in isolated perfused kidneys of the rat
Author(s) -
Ziyyat Abderrahim,
Zhang BeiLi,
Benzoni Daniel
Publication year - 1996
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1996.tb15998.x
Subject(s) - thromboxane , prostanoid , chemistry , nitric oxide , endocrinology , medicine , renal function , kidney , renal circulation , prostaglandin , renal blood flow , excretion , perfusion , platelet
1 The present study was aimed to assess the interaction between nitric oxide (NO) and thromboxane (Tx) A 2 ‐prostaglandin (PG) H 2 in single‐pass perfused isolated kidneys of the rat. 2 Noradrenaline (NA, 63 and 110 nM) dose‐dependently elevated the renal vascular resistance (RVR), the glomerular filtration rate (GFR) and the urinary excretion of sodium (U Na V). Infusion of N γ ‐nitro‐L‐arginine methyl ester (L‐NAME, 100 μ m ), an inhibitor of NO synthesis, enhanced the effects of NA on RVR and on U Na V, but decreased those on GFR. The TxA 2 ‐PGH 2 (TP) receptor blockade by GR32191B (10 μ m ) attenuated this potentiating effect of L‐NAME. 3 When renal perfusion pressure was stepwise increased from 90 to 150 mmHg, L‐NAME similarly decreased renal perfusion flow rate and GFR. 4 The venous excretion of TxB 2 and 6‐keto‐PGF 1α was increased by L‐NAME in baseline conditions as well as after NA or increasing renal perfusion pressure (RPP). 5 These results suggest that: (1) TxA 2 and PGH 2 play an important role in the overall effect of the renal prostanoids, (2) NO strongly interacts with the cyclo‐oxygenase pathway and reduces the prostanoid synthesis in the kidney, and (3) the pressor effect of L‐NAME partly relies upon the vasoconstrictor effect of TxA 2 and PGH 2 .