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Renal hemodynamic and excretory effects of n‐0861, a non‐xanthine adenosine A 1 ‐receptor antagonist
Author(s) -
Barrett Richard J.,
Wright Kathryn F.,
Droppleman David A.
Publication year - 1994
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.430320310
Subject(s) - endocrinology , medicine , antagonist , adenosine , reabsorption , chemistry , excretion , hemodynamics , adenosine receptor , receptor antagonist , excretory system , adenosine receptor antagonist , kidney , renal physiology , xanthine , natriuresis , receptor , biochemistry , enzyme , agonist
The renal hemodynamic and excretory effects of intravenous N‐0861, a non‐xanthine adenosine A 1 ‐receptor antagonist, were evaluated in conscious and anesthetized male Sprague‐Dawely rats. In conscious rats, N‐0861 (10, 30 μmol/kg, iv) significantly increased the excretion of urine, Na + , and K + ; U Cl V was increased only in the rats treated with 10 μmol/kg, N‐0861. The relative excretion of K + was similar to that of Na + . Lower doses of N‐0861 (1, 3 μmol/kg, iv) had no effect. During clearance studies in anesthetized rats, N‐0861 (3, 10, 30 μmol/kg, iv) had little effect on systemic or renal hemodynamics, but provoked significant saluresis that was poorly related to dose, and that was characterized by a somewhat greater excretion of Na + and Cl −− relative to K + . These results indicate that the selective adenosine A 1 receptor antagonist N‐0861 has little influence on resting renal hemodynamics and suggest that the natriuretic responses are due to inhibition of tubular Na + reabsorption.