PMID- 8920935
OWN - NLM
STAT- MEDLINE
DCOM- 19961230
LR  - 20141120
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 228
IP  - 2
DP  - 1996 Nov 12
TI  - Evidence for inducible nitric oxide synthase in spontaneously hypertensive rats.
PG  - 459-66
AB  - This study investigates the mechanism of the production of nitric oxide (NO) 
      caused by lipopolysaccharide (LPS) in spontaneously hypertensive rats (SHR) or 
      Wistar-Kyoto (WKY) rats. The injection of LPS (5 mg/ kg, i.v.) caused a mild 
      hypotension in WKY rats, while it induced a more severe hypotensive effect in 
      SHR. The basal level of plasma nitrite was slightly higher in SHR than in WKY 
      rats. At 3 h after injection of LPS, the increment in plasma nitrite was more 
      significant in SHR. Prior to the treatment of rats with LPS, the plasma level of 
      tumor necrosis factor-alpha (TNF alpha) was also higher in SHR than in WKY rats, 
      and LPS induced a more significant increase of TNF alpha level (at 1 h) in SHR. 
      In rats treated with LPS, acetylcholine-induced relaxation was significantly 
      impaired in thoracic aortic rings obtained from WKY rats, but not in those from 
      SHR. By contrast, L-arginine (1 mM) did not cause any relaxations in rings 
      without the endothelium obtained from WKY rats while it slightly relaxed those 
      from SHR, and this difference was further augmented by treatment of rats with LPS 
      for 3 h. In addition, the basal cGMP level was higher in SHR, which was inhibited 
      by aminoguanidine (AG, 1 mM). The treatment of rats with LPS further increased 
      the formation of cGMP in both strains and this increment was greater in SHR than 
      in WKY rats, which was also attenuated by AG to a similar level between both 
      strains. Interestingly, an expression of inducible NO synthase (NOS II) protein 
      was only observed in SHR, and further enhanced by treated rats with LPS. We 
      conclude that an increased production of NO in SHR, which was further enhanced by 
      LPS, is attributed to a basal expression of NOS II.
FAU - Wu, C C
AU  - Wu CC
AD  - Department of Pharmacology, National Defense Medical Center, Taipei, Taiwan, 
      Repbulic of China.
FAU - Hong, H J
AU  - Hong HJ
FAU - Chou, T C
AU  - Chou TC
FAU - Ding, Y A
AU  - Ding YA
FAU - Yen, M H
AU  - Yen MH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Guanidines)
RN  - 0 (Isoenzymes)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Nitrites)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 94ZLA3W45F (Arginine)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - H2D2X058MU (Cyclic GMP)
RN  - N9YNS0M02X (Acetylcholine)
RN  - SCQ4EZQ113 (pimagedine)
RN  - TBT296U68M (1-Methyl-3-isobutylxanthine)
SB  - IM
MH  - 1-Methyl-3-isobutylxanthine/pharmacology
MH  - Acetylcholine/pharmacology
MH  - Animals
MH  - Aorta, Thoracic/drug effects/physiology/physiopathology
MH  - Arginine/pharmacology
MH  - Blood Pressure/drug effects
MH  - Cyclic GMP/metabolism
MH  - Enzyme Induction
MH  - Guanidines/pharmacology
MH  - In Vitro Techniques
MH  - Isoenzymes/biosynthesis/metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - Muscle Contraction/drug effects
MH  - Muscle, Smooth, Vascular/drug effects/*physiology/physiopathology
MH  - Nitric Oxide Synthase/biosynthesis/*metabolism
MH  - Nitrites/blood
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 1996/11/12 00:00
MHDA- 1996/11/12 00:01
CRDT- 1996/11/12 00:00
PHST- 1996/11/12 00:00 [pubmed]
PHST- 1996/11/12 00:01 [medline]
PHST- 1996/11/12 00:00 [entrez]
AID - S0006-291X(96)91682-4 [pii]
AID - 10.1006/bbrc.1996.1682 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 1996 Nov 12;228(2):459-66. doi: 
      10.1006/bbrc.1996.1682.