PMID- 22139055
OWN - NLM
STAT- MEDLINE
DCOM- 20121010
LR  - 20211021
IS  - 1437-7799 (Electronic)
IS  - 1342-1751 (Linking)
VI  - 16
IP  - 3
DP  - 2012 Jun
TI  - The actions of Shiga toxin-2 administration into the brain on renal sympathetic 
      nerve activity.
PG  - 382-8
LID - 10.1007/s10157-011-0572-4 [doi]
AB  - BACKGROUND: It remains unclear whether Shiga toxin-2 (Stx-2)-induced acute 
      encephalopathy contributes to an inappropriate activation of the renal 
      sympathetic outflow. This investigation set out to examine the impact of Stx-2 
      administered into the brain on the neural control of the kidney. METHODS: Using 
      acutely anaesthetised male Wistar rats (300-350 g), saline, Stx-2 (10 mug/kg) or 
      lipopolysaccharide (LPS 50 mug/kg) was administered intracerebroventricularly 
      (icv) and measurements of renal haemodynamic and excretory function or renal 
      nerve activity were made over the following 4 h. RESULTS: There were minimal 
      changes in renal blood flow, glomerular filtration rate, urine flow or sodium 
      excretion, irrespective of whether saline, Stx-2 or LPS was administered into the 
      brain. The renal nerve recordings showed that whereas saline and LPS caused small 
      inconsistent changes in renal nerve activity over the 4-h period, there was a 
      significant (P < 0.05) doubling of renal nerve activity in the rats which were 
      administered Stx-2 icv. Immunocytochemical examination demonstrated that Stx-2 
      induced globotriaosylceramide receptors, the proposed functional receptors for 
      Stx-2, on the blood vessel walls around the hypothalamus and hippocampus, and 
      histological evaluations showed that changes in the kidney were beginning to 
      occur to the renal tubular epithelial cells, consistent with developing lesions. 
      CONCLUSION: Stx-2 crosses either the blood-brain barrier or the 
      blood-cerebrospinal fluid barrier where it can alter neuronal function and 
      trigger neuronal derangements. These structural changes could contribute, at 
      least in part, to the raised renal sympathetic nerve activity.
FAU - Nakamura, Akio
AU  - Nakamura A
AD  - Department of Paediatrics, School of Medicine, Teikyo University, Tokyo, Japan. 
      akio@med.teikyo-u.ac.jp
FAU - Imaizumi, Akira
AU  - Imaizumi A
FAU - Kohsaka, Takao
AU  - Kohsaka T
FAU - Huang, Chunlong
AU  - Huang C
FAU - Huang, Chunhua
AU  - Huang C
FAU - Johns, Edward J
AU  - Johns EJ
LA  - eng
PT  - Journal Article
DEP - 20111203
PL  - Japan
TA  - Clin Exp Nephrol
JT  - Clinical and experimental nephrology
JID - 9709923
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Shiga Toxin 2)
SB  - IM
MH  - Animals
MH  - Blood Pressure/drug effects
MH  - Blood-Brain Barrier/physiology
MH  - Injections, Intraventricular
MH  - Kidney/drug effects/*innervation/pathology
MH  - Lipopolysaccharides/toxicity
MH  - Male
MH  - Rats
MH  - Rats, Wistar
MH  - Renal Circulation/drug effects
MH  - Shiga Toxin 2/*toxicity
MH  - Sympathetic Nervous System/drug effects/*physiology
EDAT- 2011/12/06 06:00
MHDA- 2012/10/12 06:00
CRDT- 2011/12/06 06:00
PHST- 2011/08/04 00:00 [received]
PHST- 2011/11/16 00:00 [accepted]
PHST- 2011/12/06 06:00 [entrez]
PHST- 2011/12/06 06:00 [pubmed]
PHST- 2012/10/12 06:00 [medline]
AID - 10.1007/s10157-011-0572-4 [doi]
PST - ppublish
SO  - Clin Exp Nephrol. 2012 Jun;16(3):382-8. doi: 10.1007/s10157-011-0572-4. Epub 2011 
      Dec 3.