PMID- 17184505
OWN - NLM
STAT- MEDLINE
DCOM- 20070123
LR  - 20131121
IS  - 0305-1870 (Print)
IS  - 0305-1870 (Linking)
VI  - 33
IP  - 12
DP  - 2006 Dec
TI  - Renal denervation attenuates long-term hypertensive effects of Angiotensin ii in 
      the rat.
PG  - 1225-30
AB  - 1. It is well accepted that some of the long-term effects of angiotensin (Ang) II 
      are mediated via the central nervous system. Some of these actions that are 
      mediated by the circumventricular organs and the baroreceptor reflex are thought 
      to then alter sympathetic nervous system activity. In particular, there is some 
      debate as to the role of renal nerves in the chronic effects of AngII. The aim of 
      the present study was to assess the contribution of the renal nerves in a 
      long-term model of progressive AngII-induced hypertension. 2. Male Sprague-Dawley 
      rats were subjected to either bilateral renal denervation (RDX; n = 7) or sham 
      surgery (SHAM; n = 8). Rats were instrumented with radiotelemetric transducers 
      and venous catheters for the measurement of blood pressure and AngII infusion, 
      respectively. A 4.0% NaCl diet and distilled water were provided ad libitum. The 
      first 3 days served as the control period (7 mL/day, 0.9% NaCl, i.v.). This was 
      followed by an infusion of AngII for 16 days (10 ng/kg per min, i.v.) and a 3 day 
      recovery period identical to control. 3. Baseline arterial pressure between RDX 
      and SHAM rats did not differ. Following AngII treatment, the arterial pressure of 
      SHAM rats increased more rapidly than that of RDX rats. By Day 10 of treatment, 
      the mean arterial pressure was significantly different between groups, having 
      increased to 166 +/- 4 mmHg in SHAM rats and 135 +/- 11 mmHg in RDX rats. This 
      trend continued for the remainder of AngII treatment. 4. The present results 
      indicate that the renal nerves are necessary for the full expression of 
      AngII-induced hypertension.
FAU - Hendel, Michael D
AU  - Hendel MD
AD  - Department of Veterinary and Biomedical Sciences, University of Minnesota, St 
      Paul, MN 55108, USA. hend0450@umn.edu
FAU - Collister, John P
AU  - Collister JP
LA  - eng
GR  - R01 HL072180/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - Australia
TA  - Clin Exp Pharmacol Physiol
JT  - Clinical and experimental pharmacology & physiology
JID - 0425076
RN  - 11128-99-7 (Angiotensin II)
RN  - 9NEZ333N27 (Sodium)
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
MH  - Angiotensin II/*pharmacology
MH  - Animals
MH  - Blood Pressure/drug effects
MH  - Denervation
MH  - Drinking/drug effects
MH  - Eating/drug effects
MH  - Heart Rate/drug effects
MH  - Hypertension/*chemically induced/physiopathology
MH  - Kidney/*innervation/metabolism/physiology
MH  - Male
MH  - Norepinephrine/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sodium/urine
MH  - Urodynamics/drug effects
MH  - Water-Electrolyte Balance/physiology
EDAT- 2006/12/23 09:00
MHDA- 2007/01/24 09:00
CRDT- 2006/12/23 09:00
PHST- 2006/12/23 09:00 [pubmed]
PHST- 2007/01/24 09:00 [medline]
PHST- 2006/12/23 09:00 [entrez]
AID - CEP4514 [pii]
AID - 10.1111/j.1440-1681.2006.04514.x [doi]
PST - ppublish
SO  - Clin Exp Pharmacol Physiol. 2006 Dec;33(12):1225-30. doi: 
      10.1111/j.1440-1681.2006.04514.x.