PMID- 11300659
OWN - NLM
STAT- MEDLINE
DCOM- 20011011
LR  - 20190724
IS  - 0160-2446 (Print)
IS  - 0160-2446 (Linking)
VI  - 37
IP  - 4
DP  - 2001 Apr
TI  - Effects of bradykinin on renal nerve stimulation-induced antidiuresis and 
      norepinephrine overflow in anesthetized dogs.
PG  - 461-70
AB  - We examined effects of bradykinin on antidiuresis and norepinephrine overflow 
      induced by renal nerve stimulation (RNS) in anesthetized dogs, with or without 
      blockade of the B2 receptor by Hoe 140 (D-Arg-[Hyp3, Thi5, D-Tic7, 
      Oic8]bradykinin) or the endogenous nitric oxide generation by 
      N(G)nitro-L-arginine (NOARG), a nitric oxide synthase inhibitor. RNS (0.5-2.0 Hz) 
      produced significant decreases in urine flow, urinary and fractional excretions 
      of sodium, and increases in norepinephrine secretion rate (NESR), without 
      affecting systemic and renal hemodynamics. Intrarenal arterial infusion of 
      bradykinin (5 ng/kg per minute) significantly suppressed the RNS-induced 
      antidiuresis and increase in NESR. Hoe 140 (100 ng/kg per minute) did not affect 
      the RNS-induced renal actions, but in the presence of Hoe 140, bradykinin-induced 
      suppressive actions on reductions in urine formation and increases in NESR in 
      response to RNS were abolished. RNS during intrarenal arterial infusion of NOARG 
      (40 microg/kg per minute) led to potent reductions in urine formation and 
      decreased renal blood flow and glomerular filtration rate. Simultaneously, NESR 
      was markedly increased. During NOARG infusion, bradykinin-induced decreases in 
      renal actions elicited by RNS were markedly attenuated. These findings suggest 
      that bradykinin suppresses the RNS-induced norepinephrine overflow and renal 
      actions via nitric oxide production mediated by activation of B2 receptor. Renal 
      noradrenergic neurotransmission may be inhibited by bradykinin at the 
      prejunctional level, when its local production in the kidney is enhanced.
FAU - Tadano, K
AU  - Tadano K
AD  - Department of Pharmacology, Osaka University of Pharmaceutical Sciences, 
      Takatsuki, Japan.
FAU - Yamasaki, T
AU  - Yamasaki T
FAU - Matsumura, Y
AU  - Matsumura Y
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Adrenergic alpha-Agonists)
RN  - 0 (Adrenergic beta-Antagonists)
RN  - 0 (Bradykinin Receptor Antagonists)
RN  - 0 (Enzyme Inhibitors)
RN  - 2149-70-4 (Nitroarginine)
RN  - 7PG89G35Q7 (icatibant)
RN  - S8TIM42R2W (Bradykinin)
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
MH  - Adrenergic alpha-Agonists/metabolism
MH  - Adrenergic beta-Antagonists/pharmacology
MH  - Animals
MH  - Bradykinin/analogs & derivatives/*pharmacology
MH  - Bradykinin Receptor Antagonists
MH  - Dogs
MH  - Electric Stimulation
MH  - Enzyme Inhibitors/pharmacology
MH  - Female
MH  - Hemodynamics
MH  - Kidney/drug effects/innervation/*physiology
MH  - Male
MH  - Natriuresis
MH  - Nitroarginine/pharmacology
MH  - Norepinephrine/*metabolism
MH  - Renal Circulation/*drug effects
MH  - Urine
EDAT- 2001/04/13 10:00
MHDA- 2001/10/12 10:01
CRDT- 2001/04/13 10:00
PHST- 2001/04/13 10:00 [pubmed]
PHST- 2001/10/12 10:01 [medline]
PHST- 2001/04/13 10:00 [entrez]
AID - 10.1097/00005344-200104000-00013 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 2001 Apr;37(4):461-70. doi: 
      10.1097/00005344-200104000-00013.