PMID- 11824865
OWN - NLM
STAT- MEDLINE
DCOM- 20020716
LR  - 20190513
IS  - 0895-7061 (Print)
IS  - 0895-7061 (Linking)
VI  - 15
IP  - 1 Pt 1
DP  - 2002 Jan
TI  - Chronic treatment with a superoxide dismutase mimetic prevents vascular 
      remodeling and progression of hypertension in salt-loaded stroke-prone 
      spontaneously hypertensive rats.
PG  - 78-84
AB  - Oxidative stress has been implicated in the pathogenesis of hypertension. The aim 
      of the present study was to determine whether increased generation of vascular 
      superoxide anion (*O2-) contributes to blood pressure elevation by influencing 
      vascular function and structure in severely hypertensive rats. Sixteen-week-old 
      stroke-prone spontaneously hypertensive rats (SHRSP) (n = 12) were randomly 
      divided into two groups to receive the superoxide dismutase mimetic, tempol 
      (4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl) (1 mmol/L in drinking water) or tap 
      water. Both groups were fed a high-salt diet (4% NaCl). Systolic blood pressure 
      (SBP) was measured weekly for 6 weeks by the tail-cuff method. Rats were killed, 
      and vascular structure (media:lumen ratio) and endothelial function 
      (acetylcholine [Ach]-induced vasodilation) were assessed in small mesenteric 
      arteries mounted as pressurized preparations. Vascular *O2- concentration was 
      measured by lucigenin (5 micromol/L) chemiluminescence. Plasma total antioxidant 
      status was assessed spectrophotometrically. The SBP increased significantly (P < 
      .01) in the control group, whereas progression of hypertension was prevented in 
      the tempol-treated group. Tempol reduced (P < .01) the media:lumen ratio 
      (7.2%+/-0.01%) compared with that in controls (12.0%+/-0.01%). Maximal 
      Ach-induced dilation was altered in control rats (40%+/-9%) but was not 
      influenced by tempol (57%+/-17%). Vascular *O2- concentration was lower (P < .01) 
      and plasma total antioxidant concentration was higher (P < .05) in the treated 
      group compared with the control. In conclusion, tempol prevents progression of 
      hypertension. These processes are associated with attenuated vascular remodeling, 
      decreased vascular *O2- concentration, and increased antioxidant status. Our data 
      suggest that oxidative stress plays an important role in vascular damage 
      associated with severe hypertension in salt-loaded SHRSP.
FAU - Park, Jeong Bae
AU  - Park JB
AD  - Clinical Research Institute of Montreal, University of Montreal, Quebec, Canada.
FAU - Touyz, Rhian M
AU  - Touyz RM
FAU - Chen, Xin
AU  - Chen X
FAU - Schiffrin, Ernesto L
AU  - Schiffrin EL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Hypertens
JT  - American journal of hypertension
JID - 8803676
RN  - 0 (Antioxidants)
RN  - 0 (Cyclic N-Oxides)
RN  - 0 (Sodium Chloride, Dietary)
RN  - 0 (Spin Labels)
RN  - 0 (Vasodilator Agents)
RN  - 11062-77-4 (Superoxides)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - N9YNS0M02X (Acetylcholine)
RN  - U78ZX2F65X (tempol)
SB  - IM
MH  - Acetylcholine/pharmacology
MH  - Animals
MH  - Antioxidants/*pharmacology
MH  - Blood Pressure/drug effects
MH  - Cyclic N-Oxides/*pharmacology
MH  - Hypertension, Malignant/chemically induced/*drug therapy/*pathology
MH  - Male
MH  - Mesenteric Arteries/metabolism/pathology
MH  - Oxidative Stress/drug effects
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Sodium Chloride, Dietary/pharmacology
MH  - Spin Labels
MH  - Stroke/etiology
MH  - Superoxide Dismutase/*metabolism
MH  - Superoxides/blood
MH  - Vasodilation/drug effects
MH  - Vasodilator Agents/pharmacology
EDAT- 2002/02/05 10:00
MHDA- 2002/07/18 10:01
CRDT- 2002/02/05 10:00
PHST- 2002/02/05 10:00 [pubmed]
PHST- 2002/07/18 10:01 [medline]
PHST- 2002/02/05 10:00 [entrez]
AID - S0895706101022336 [pii]
AID - 10.1016/s0895-7061(01)02233-6 [doi]
PST - ppublish
SO  - Am J Hypertens. 2002 Jan;15(1 Pt 1):78-84. doi: 10.1016/s0895-7061(01)02233-6.