Enhancement of Norepinephrine and Angiotensin II-Induced Renal Effects by NG-Nitro-L-arginine, a Nitric Oxide Synthase Inhibitor

• Published in: Biological & pharmaceutical bulletin Vol. 18; no. 4; pp. 496 - 500
• Main Authors: MATSUMURA, Yasuo, EGI, Yasuhiro, MAEKAWA, Hitoshi, MIURA, Akihisa, MURATA, Satoshi, MORIMOTO, Shiro
• Format: Journal Article
• Language: English
• Published: Tokyo The Pharmaceutical Society of Japan 1995; Maruzen; Japan Science and Technology Agency
• Subjects: Amino Acid Oxidoreductases - antagonists & inhibitors; Anesthesia; angiotensin II; Angiotensin II - pharmacology; Animals; Arginine - analogs & derivatives; Arginine - pharmacology; Biological and medical sciences; Denervation; Dogs; Drug Synergism; Female; Glomerular Filtration Rate - drug effects; Hemodynamics - drug effects; Kidney - drug effects; Kidney - innervation; Kidney Function Tests; Male; Medical sciences; NG-nitro-L-arginine; nitric oxide; Nitric Oxide - antagonists & inhibitors; Nitric Oxide Synthase; Nitroarginine; norepinephrine; Norepinephrine - pharmacology; Pharmacology. Drug treatments; Renal Circulation - drug effects; renal vasoconstriction; Urinary system; urine formation; Fissipedia; Carnivora; Peptide hormone; Kidney; Renin angiotensin system; Vertebrata; Mammalia; Animal; Nitrogen monoxide; Norepinephrine; Hemodynamics; Angiotensin II; Dog
• ISSN: 0918-6158; 1347-5215
• DOI: 10.1248/bpb.18.496

We investigated whether endogenous nitric oxide (NO) has a role as an inhibitory modulator of norepinephrine (NE)- and angiotensin II (Ang II)-induced renal effects in anesthetized dogs. Intrarenal arterial infusion of NE (100 ng/kg/min) or Ang II (10 ng/kg/min) decreased renal blood flow (RBF), glomerular filtration rate (GFR) and urine formation. The NE- or Ang II-induced renal effects were augmented by the intrarenal administration of a NO synthase inhibitor, NG-nitro-L-arginine (NOARG), at doses (10 and 40 μg/kg/min) which did not affect the mean arterial blood pressure and heart rate. The stimulating activity of NOARG on NE- or Ang II-induced renal effects were abolished by the simultaneous administration of L-arginine, a NO precursor. These findings suggest that endogenous NO, which is probably generated within the kidney, functions as an inhibitory modulator in NE- or Ang II-induced renal vasoconstriction and antidiuresis.