Angiotensin II-induced renal responses in anesthetized rabbits: Effects of N(ω)-nitro-L-arginine methyl ester and losartan

Yuichiro Adachi, Kazuyuki Hashimoto, Hiroaki Hisa, Makoto Yoshida, Mizue Suzuki-Kusaba, Susumu Satoh

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Intrarenal arterial infusion of angiotensin II (4 ng/kg/min) reduced renal blood flow, glomerular filtration rate and urinary Na+ excretion (UNaV) without affecting fractional Na+ excretion (FENa) in anesthetized rabbits. Losartan (10 μg/kg/min) abolished these angiotensin II-induced renal responses. The renal blood flow, glomerular filtration rate and UNaV responses were potentiated during intrarenal arterial infusion of N(ω)-nitro-L-arginine methyl ester (L-NAME, 10 μg/kg/min). A high dose of L-NAME (50 μg/kg/min) also potentiated the renal blood flow and UNaV responses but not the glomerular filtration rate response. Angiotensin II reduced FENa during L-NAME infusion at either dose. In L-NAME-pretreated rabbits, losartan abolished the angiotensin II-induced renal blood flow and glomerular filtration rate responses, but the reduction in FENa still remained. The present study suggests that in the rabbit kidney (1) nitric oxide attenuates the angiotensin II-induced (angiotensin ATl receptor-mediated) vasoconstriction and (2) angiotensin II can evoke losartan-resistant tubular Na+ reabsorption, but the tubular action is concealed by nitric oxide.

Original languageEnglish
Pages (from-to)165-171
Number of pages7
JournalEuropean Journal of Pharmacology
Volume308
Issue number2
DOIs
Publication statusPublished - 1996 Jul 18

Keywords

  • L-NAME (N(ω)-nitro-L-arginine methyl ester)
  • angiotensin II
  • kidney
  • losartan
  • nitric oxide (NO)
  • rabbit

ASJC Scopus subject areas

  • Pharmacology

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