Nitric oxide modulates renal actions of NKH477 in the anesthetized dogs

• Published in: Japanese Journal of Pharmacology 1999, Vol.79 (suppl.2), p.267-267
• Main Authors: Sunao Hara, Masayuki Tanahasi, Kazutomo Saitoh, Hiroaki Hisa, Susumu Satoh
• Format: Article
• Language: Japanese
• ISSN: 0021-5198

We had previously reported that NKH477, an adenylate cyclase activator, caused diuresis and natriuresis in anesthetized dogs (The 71st Annual Meet-ing of The Japanese Pharmacological Society, 1998). On the present study, we examined weather the renal actions of NKH477 are modulated by the nitric oxide (NO) system.NKH477 was infused into the renal artery before and during intrarenal arterial infusion of a spontaneous NO donor NOC7 or a NO synthase inhibitor L-NAME. NKH477 (300 ng/kg/min) increased renal blood flow (RBF), glomerular filtration rate (GFR), urine flow rate (UV), urinary sodium excretion (UNaV) and fractional sodium excretion (FENa). NOC7 (30 ng/kg/min) had little influence on basal values of these renal parameters. L-NAME (10 and 50 μg/kg/min) decreased basal RBF, GFR, UV, UNaV, FENa and uri-nary NOx excretion. The increasing effects of NKH477 on UV, UNaV and FENa were attenu-ated in the presence of NOC7 and enhanced in the presence of L-NAME. However, the NKH477-induced increases in RBF and GFR remained un changed. These results suggest that the NO system regulates cAMP-mediated inhi-bition of tubular reabsorption in the dog kidney.