PMID- 11139367
OWN - NLM
STAT- MEDLINE
DCOM- 20010222
LR  - 20161020
IS  - 1089-8603 (Print)
IS  - 1089-8603 (Linking)
VI  - 4
IP  - 6
DP  - 2000 Dec
TI  - Nitric oxide synthase activity in retinas from non-insulin-dependent diabetic 
      Goto-Kakizaki rats: correlation with blood-retinal barrier permeability.
PG  - 590-6
AB  - The aim of this work was to examine whether the non-insulin-dependent diabetic 
      Goto-Kakizaki (GK) rats develop retinal changes with similar characteristics to 
      those observed in insulin-dependent diabetic rats in what concerns blood-retinal 
      barrier (BRB) permeability, nitric oxide (NO) production, and retinal IL-1beta 
      level. BRB permeability was evaluated by vitreous fluorophotometry. NO synthase 
      (NOS) activity was assessed by the production of l-[(3)H]-citrulline and retinal 
      IL-1beta level was determined by ELISA. The expression of the inducible isoform 
      of NOS (iNOS) protein was evaluated by Western blot analysis and 
      immunohistochemistry. The in vivo studies indicated that in GK rats the BRB 
      permeability to fluorescein was increased (787.81 +/- 68 min(-1)) in comparison 
      to that in normal Wistar rats (646.6 +/- 55 min(-1)). The ex vivo studies showed 
      that in retinas from GK rats the NOS activity was higher (207 +/- 28.9 pmol 
      l-[(3)H]-citrulline/mg protein/30 min) than that in normal Wistar rats (125 +/- 
      32.3 pmol l-[(3)H]-citrulline/mg protein/30 min). These results were correlated 
      with an increase in the protein level of iNOS in the retinas of GK rats, which 
      was confirmed not only by the study of the iNOS protein expression but also by 
      the use of NOS activity inhibitors. Indeed, the data about the effect of specific 
      inhibitors on the NOS activity revealed that in retinas from GK rats the most 
      effective inhibitor was aminoguanidine, which predominantly inhibits the iNOS 
      isoform whereas in retinas from normal Wistar rats it was N(G) nitro l-arginine 
      that predominantly inhibits the constitutive isoforms of NOS. In summary, in 
      retinas from GK rats there is an increased production of NO which may contribute 
      to the BRB breakdown.
CI  - Copyright 2000 Academic Press.
FAU - Carmo, A
AU  - Carmo A
AD  - Center of Opthalmology, Institute for Biomedical Research on Light and Image, 
      University of Coimbra, Coimbra, Portugal. analia@imagem.ibili.uc.pt
FAU - Cunha-Vaz, J G
AU  - Cunha-Vaz JG
FAU - Carvalho, A P
AU  - Carvalho AP
FAU - Lopes, M C
AU  - Lopes MC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Nitric Oxide
JT  - Nitric oxide : biology and chemistry
JID - 9709307
RN  - 0 (Blood Glucose)
RN  - 0 (Guanidines)
RN  - 0 (Interleukin-1)
RN  - 2149-70-4 (Nitroarginine)
RN  - 94ZLA3W45F (Arginine)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.13.39 (Nos2 protein, rat)
RN  - SCQ4EZQ113 (pimagedine)
SB  - IM
MH  - Animals
MH  - Arginine/metabolism/pharmacokinetics
MH  - Blood Glucose
MH  - Blood-Retinal Barrier/drug effects/*physiology
MH  - Blotting, Western
MH  - Densitometry
MH  - Diabetes Mellitus, Experimental/complications/*enzymology
MH  - Diabetes Mellitus, Type 2/complications/*enzymology
MH  - Diabetic Retinopathy/*enzymology/etiology/pathology
MH  - Disease Models, Animal
MH  - Fluorescein Angiography
MH  - Guanidines/pharmacology
MH  - Immunohistochemistry
MH  - Interleukin-1/metabolism
MH  - Nitric Oxide Synthase/*metabolism
MH  - Nitric Oxide Synthase Type II
MH  - Nitroarginine/pharmacology
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Rats, Wistar
MH  - Retina/enzymology/pathology
MH  - Retinal Vessels/drug effects/metabolism/pathology
EDAT- 2001/01/05 11:00
MHDA- 2001/03/03 10:01
CRDT- 2001/01/05 11:00
PHST- 2001/01/05 11:00 [pubmed]
PHST- 2001/03/03 10:01 [medline]
PHST- 2001/01/05 11:00 [entrez]
AID - S1089-8603(00)90312-4 [pii]
AID - 10.1006/niox.2000.0312 [doi]
PST - ppublish
SO  - Nitric Oxide. 2000 Dec;4(6):590-6. doi: 10.1006/niox.2000.0312.