PMID- 16718509
OWN - NLM
STAT- MEDLINE
DCOM- 20070111
LR  - 20191210
IS  - 0031-6768 (Print)
IS  - 0031-6768 (Linking)
VI  - 452
IP  - 6
DP  - 2006 Sep
TI  - Expression and activity of the glutamate transporter EAAT2 in cardiac 
      hypertrophy: implications for ischaemia reperfusion injury.
PG  - 674-82
AB  - The expression and activity of the glutamate transporter, excitatory amino acid 
      transporter 2 (EAAT2), in cardiac hypertrophy were investigated with respect to 
      glutamate's potential as a cardioprotective agent. Sarcolemmal vesicles (SV) 
      isolated from hypertrophic hearts of male spontaneously hypertensive rats (SHR) 
      or normotrophic hearts from age-matched male Wistar Kyoto rats (WKY) were used to 
      measure the relative level of EAAT2 expression by Western blotting and the 
      initial rate of 0-0.3 mM L-[(14)C]glutamate uptake. The effects of 20-min global 
      normothermic ischaemia +/-0.5 mM glutamate on cardiac function were measured in 
      isolated working SHR/WKY hearts. In a separate series of hearts, glutamate, 
      lactate and ATP levels were measured. Both the level of EAAT2 expression and the 
      V (max) for sodium-dependent L-[(14)C]glutamate uptake were significantly greater 
      in SHR SV compared to WKY SV. The reperfusion cardiac output (CO) of SHR hearts 
      was significantly worse than that of the WKY hearts (24.3+/-2.2 ml/min vs 
      39.8+/-3.3 ml/min, n=7/9+/-SE, p<0.01). The addition of 0.5 mM L-glutamate 
      improved the SHR reperfusion CO to 45.2+/-5 ml/min, (n=6+/-SE, p<0.01) but had no 
      effect on WKYs (46.2+/-3.8 ml/min, n=6+/-SE). SHR with 0.5 mM L-glutamate had 
      higher glutamate levels at the start of ischaemia, plus higher glutamate and ATP 
      levels at the end of ischaemia compared to any other group. These results suggest 
      that increased glutamate transporter expression and activity in the SHR hearts 
      helped facilitate glutamate entry into the SHR cardiomyocytes leading to improved 
      myocardial metabolism during ischaemia and better functional recovery on 
      reperfusion.
FAU - King, Nicola
AU  - King N
AD  - Bristol Heart Institute, Department of Clinical Science at South Bristol, 
      University of Bristol, Bristol Royal Infirmary, Bristol BS2 8HW, UK. 
      n.king@bris.ac.uk
FAU - Lin, Hua
AU  - Lin H
FAU - McGivan, John D
AU  - McGivan JD
FAU - Suleiman, M Saadeh
AU  - Suleiman MS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060523
PL  - Germany
TA  - Pflugers Arch
JT  - Pflugers Archiv : European journal of physiology
JID - 0154720
RN  - 0 (Cardiotonic Agents)
RN  - 0 (Excitatory Amino Acid Transporter 2)
RN  - 0 (Slc1a2 protein, rat)
RN  - 33X04XA5AT (Lactic Acid)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - 9NEZ333N27 (Sodium)
RN  - EC 3.6.1.- (Atp1a1 protein, rat)
RN  - EC 7.2.2.13 (Sodium-Potassium-Exchanging ATPase)
SB  - IM
MH  - Adenosine Triphosphate/metabolism
MH  - Animals
MH  - Cardiac Output/physiology
MH  - Cardiomegaly/metabolism/*physiopathology
MH  - Cardiotonic Agents
MH  - Excitatory Amino Acid Transporter 2/*biosynthesis/genetics/*physiology
MH  - Glutamic Acid/metabolism/pharmacology
MH  - In Vitro Techniques
MH  - Lactic Acid/metabolism
MH  - Myocardial Reperfusion Injury/metabolism/*physiopathology
MH  - Perfusion
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Sarcolemma/metabolism
MH  - Sodium/physiology
MH  - Sodium-Potassium-Exchanging ATPase/metabolism
EDAT- 2006/05/24 09:00
MHDA- 2007/01/12 09:00
CRDT- 2006/05/24 09:00
PHST- 2006/01/19 00:00 [received]
PHST- 2006/04/19 00:00 [accepted]
PHST- 2006/04/05 00:00 [revised]
PHST- 2006/05/24 09:00 [pubmed]
PHST- 2007/01/12 09:00 [medline]
PHST- 2006/05/24 09:00 [entrez]
AID - 10.1007/s00424-006-0096-z [doi]
PST - ppublish
SO  - Pflugers Arch. 2006 Sep;452(6):674-82. doi: 10.1007/s00424-006-0096-z. Epub 2006 
      May 23.