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Clinical Studies |
Department of Medicine (To. S., S.I.), Jichi Medical School, Tochigi; Second Department of Medicine (K.A.), Tohoku University School of Medicine, Sendai; Department of Medicine (K.K.), Nagaoka Red Cross Hospital, Nagaoka; Department of Medicine (K.Y.), National Sakura Hospital, Sakura; Department of Medicine (K.S.), Tokyo Rosai Hospital, Tokyo; Department of Medicine (Ta. S.), Keio University School of Medicine, Tokyo; Second Department of Medicine (S.Y.), Chiba University School of Medicine, Chiba, Japan
Address all correspondence and requests for reprints to: Toshikazu Saito, M.D., Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical School, 3311-1 Yakushiji Minamikawachi, Tochigi 329-04 Japan.
The present study was undertaken to determine whether the nonpeptide V2 arginine vasopressin (AVP) antagonist 5-dimethylamino-1[4-(2-methylbenzoylamino)benzoyl]-2,3,4,5-tetrahydro-1H-benzazepine hydrochloride (OPC-31260) produces water diuresis and improves hyponatremia in patients with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Eleven patients (9 males and 2 females, 64 ± 3.5 yr) with SIADH were included in the present protocol, which was comprised of 3 successive days. Day 1 was a control day, and on days 2 and 3 OPC-31260 was administered intravenously. Five blood and urine collections were made at 1–2 h intervals during the 6 h observation period each day. A single administration of 0.25 and 0.5 mg/kg OPC-31260 increased the 4 h cumulative urine volume and decreased urinary osmolality to below 225 mOsm/kg H2O. Such a diuretic effect was independent of an increase in urinary solute excretions. This aquaresis by 0.5 mg/kg OPC-31260 caused a significant increase in serum sodium level by approximately 3 mEq/L. The antagonistic effect of OPC-31260 lasted for 4 h when it was given intravenously. These results indicate that OPC-31260 is an effective therapeutic agent for hyponatremia in patients with SIADH.
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