PMID- 8720419
OWN - NLM
STAT- MEDLINE
DCOM- 19961112
LR  - 20190724
IS  - 0160-2446 (Print)
IS  - 0160-2446 (Linking)
VI  - 27
IP  - 2
DP  - 1996 Feb
TI  - Effect of sodium nitroprusside on norepinephrine overflow and antidiuresis 
      induced by stimulation of renal nerves in anesthetized dogs.
PG  - 211-7
AB  - To investigate the role of nitric oxide (NO) in the regulation of renal 
      sympathetic nerve activity and renal function, we examined the effect of sodium 
      nitroprusside (SNP), a NO donor, on renal actions induced by renal nerve 
      stimulation (RNS) in anesthetized dogs, with or without blockade of an endogenous 
      NO generation by NG-nitro-L-arginine (NOARG), a NO synthase inhibitor. 
      Low-frequency RNS (0.5-2.0 Hz) enhanced the rate of norepinephrine secretion rate 
      (NESR) from the kidney and decreased urine flow (UF), urinary excretion of sodium 
      (U(Na)V), and fractional excretion of sodium (FENa, without affecting systemic 
      and renal hemodynamics. The intrarenal arterial infusion of SNP, in a dose (1 mu 
      g/kg/min) that does not affect renal hemodynamics and urine formation at the 
      basal level, significantly attenuated the RNS-induced decreases in UF, UNa V and 
      FENa. The intrarenal administration of NOARG (40 mu g/kg/min) elicited renal 
      vasoconstriction and reduced urine formation. RNS during NOARG administration 
      reduced renal blood flow (RBF) and glomerular filtration rate (GFR) and augmented 
      RNS-induced reduction in urine formation. Simultaneously, NESR was markedly 
      enhanced. The renal actions observed with NOARG administration during control and 
      RNS periods were almost completely abolished by treatment with SNP. Therefore, we 
      suggest that NO plays an important role in the regulation of renal function. 
      Endogenous NO probably functions as an inhibitory modulator of renal 
      noradrenergic neurotransmission at the prejunctional level.
FAU - Maekawa, H
AU  - Maekawa H
AD  - Department of Pharmacology, Osaka University of Pharmaceutical Sciences, 
      Matsubara, Japan.
FAU - Matsumura, Y
AU  - Matsumura Y
FAU - Matsuo, G
AU  - Matsuo G
FAU - Morimoto, S
AU  - Morimoto S
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Vasodilator Agents)
RN  - 169D1260KM (Nitroprusside)
RN  - 2149-70-4 (Nitroarginine)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
MH  - Adrenergic Fibers/*drug effects/physiology
MH  - Animals
MH  - Brachial Artery
MH  - Diuresis/*drug effects
MH  - Dogs
MH  - Electric Stimulation
MH  - Female
MH  - Glomerular Filtration Rate
MH  - Hemodynamics/physiology
MH  - Male
MH  - Natriuresis/drug effects
MH  - Nitric Oxide/*physiology
MH  - Nitroarginine/*pharmacology
MH  - Nitroprusside/*pharmacology
MH  - Norepinephrine/*metabolism
MH  - Renal Artery/*innervation
MH  - Vasodilator Agents/*pharmacology
EDAT- 1996/02/01 00:00
MHDA- 1996/02/01 00:01
CRDT- 1996/02/01 00:00
PHST- 1996/02/01 00:00 [pubmed]
PHST- 1996/02/01 00:01 [medline]
PHST- 1996/02/01 00:00 [entrez]
AID - 10.1097/00005344-199602000-00006 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 1996 Feb;27(2):211-7. doi: 
      10.1097/00005344-199602000-00006.