Brain nitric oxide synthase activity in normal, hypertensive, and stroke-prone rats

Nathalie Clavier, Joseph R. Tobin, Jeffrey Kirsch, Makoto Izuta, Richard J. Traystman

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Background and Purpose Nitric oxide-mediated cerebral vasodilation is altered in spontaneously hypertensive stroke-prone rats. Stroke predisposition in this strain could be related to a genetic defect of brain nitric oxide synthase, the enzyme responsible for nitric oxide production. We tested the hypothesis that brain nitric oxide synthase activity is altered in spontaneously hypertensive stroke-prone rats compared with spontaneously hypertensive or Wistar-Kyoto rats. Methods A colony of spontaneously hypertensive strokeprone rats was bred, in which the rate of neurological events under salt load was assessed. In a separate cohort of animals brain nitric oxide synthase activity was measured in spontaneously hypertensive stroke-prone rats (n=6) and in spontaneously hypertensive (n=6) and genetically related Wistar-Kyoto rats (n=6). Calcium dependency of nitric oxide synthase was also assessed in cortical brain samples from the three rat strains to determine if altered calcium-dependent activation of nitric oxide synthase was present. Results Brain nitric oxide synthase activity was highest in the cerebellum (eg, spontaneously hypertensive stroke-prone rats: Cerebral cortex, 10.6 ± 0.9; cerebellum, 50.1 ± 12.0; brain stem, 14.7±10.3 pmol/mg protein per minute); however, there was no difference among the three rat strains in any region (eg, cerebral cortex: Spontaneously hypertensive stroke-prone, 10.6 ± 0.9; spontaneously hypertensive, 10.8 ±0.5; Wistar-Kyoto, 10.9 ± 0.7 pmol/mg protein per minute) or at any calcium concentration tested. Conclusions A genetic defect of brain nitric oxide synthase is unlikely to be the cause of stroke predisposition in spontaneously hypertensive stroke-prone rats.

Original languageEnglish (US)
Pages (from-to)1674-1677
Number of pages4
JournalStroke
Volume25
Issue number8
StatePublished - 1994
Externally publishedYes

Fingerprint

Nitric Oxide Synthase
Stroke
Brain
Inbred WKY Rats
Calcium
Cerebral Cortex
Cerebellum
Nitric Oxide
Inbred SHR Rats
Vasodilation
Brain Stem
Proteins
Salts
Enzymes

Keywords

  • Cerebral ischemia
  • Focal
  • Genetics
  • Nitric oxide
  • Rats

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Clinical Neurology
  • Advanced and Specialized Nursing
  • Neuroscience(all)

Cite this

Clavier, N., Tobin, J. R., Kirsch, J., Izuta, M., & Traystman, R. J. (1994). Brain nitric oxide synthase activity in normal, hypertensive, and stroke-prone rats. Stroke, 25(8), 1674-1677.

Brain nitric oxide synthase activity in normal, hypertensive, and stroke-prone rats. / Clavier, Nathalie; Tobin, Joseph R.; Kirsch, Jeffrey; Izuta, Makoto; Traystman, Richard J.

In: Stroke, Vol. 25, No. 8, 1994, p. 1674-1677.

Research output: Contribution to journalArticle

Clavier, N, Tobin, JR, Kirsch, J, Izuta, M & Traystman, RJ 1994, 'Brain nitric oxide synthase activity in normal, hypertensive, and stroke-prone rats', Stroke, vol. 25, no. 8, pp. 1674-1677.
Clavier N, Tobin JR, Kirsch J, Izuta M, Traystman RJ. Brain nitric oxide synthase activity in normal, hypertensive, and stroke-prone rats. Stroke. 1994;25(8):1674-1677.
Clavier, Nathalie ; Tobin, Joseph R. ; Kirsch, Jeffrey ; Izuta, Makoto ; Traystman, Richard J. / Brain nitric oxide synthase activity in normal, hypertensive, and stroke-prone rats. In: Stroke. 1994 ; Vol. 25, No. 8. pp. 1674-1677.
@article{9b77e0776dc44ef9ba02b2845da577e9,
title = "Brain nitric oxide synthase activity in normal, hypertensive, and stroke-prone rats",
abstract = "Background and Purpose Nitric oxide-mediated cerebral vasodilation is altered in spontaneously hypertensive stroke-prone rats. Stroke predisposition in this strain could be related to a genetic defect of brain nitric oxide synthase, the enzyme responsible for nitric oxide production. We tested the hypothesis that brain nitric oxide synthase activity is altered in spontaneously hypertensive stroke-prone rats compared with spontaneously hypertensive or Wistar-Kyoto rats. Methods A colony of spontaneously hypertensive strokeprone rats was bred, in which the rate of neurological events under salt load was assessed. In a separate cohort of animals brain nitric oxide synthase activity was measured in spontaneously hypertensive stroke-prone rats (n=6) and in spontaneously hypertensive (n=6) and genetically related Wistar-Kyoto rats (n=6). Calcium dependency of nitric oxide synthase was also assessed in cortical brain samples from the three rat strains to determine if altered calcium-dependent activation of nitric oxide synthase was present. Results Brain nitric oxide synthase activity was highest in the cerebellum (eg, spontaneously hypertensive stroke-prone rats: Cerebral cortex, 10.6 ± 0.9; cerebellum, 50.1 ± 12.0; brain stem, 14.7±10.3 pmol/mg protein per minute); however, there was no difference among the three rat strains in any region (eg, cerebral cortex: Spontaneously hypertensive stroke-prone, 10.6 ± 0.9; spontaneously hypertensive, 10.8 ±0.5; Wistar-Kyoto, 10.9 ± 0.7 pmol/mg protein per minute) or at any calcium concentration tested. Conclusions A genetic defect of brain nitric oxide synthase is unlikely to be the cause of stroke predisposition in spontaneously hypertensive stroke-prone rats.",
keywords = "Cerebral ischemia, Focal, Genetics, Nitric oxide, Rats",
author = "Nathalie Clavier and Tobin, {Joseph R.} and Jeffrey Kirsch and Makoto Izuta and Traystman, {Richard J.}",
year = "1994",
language = "English (US)",
volume = "25",
pages = "1674--1677",
journal = "Stroke",
issn = "0039-2499",
publisher = "Lippincott Williams and Wilkins",
number = "8",

}

TY - JOUR

T1 - Brain nitric oxide synthase activity in normal, hypertensive, and stroke-prone rats

AU - Clavier, Nathalie

AU - Tobin, Joseph R.

AU - Kirsch, Jeffrey

AU - Izuta, Makoto

AU - Traystman, Richard J.

PY - 1994

Y1 - 1994

N2 - Background and Purpose Nitric oxide-mediated cerebral vasodilation is altered in spontaneously hypertensive stroke-prone rats. Stroke predisposition in this strain could be related to a genetic defect of brain nitric oxide synthase, the enzyme responsible for nitric oxide production. We tested the hypothesis that brain nitric oxide synthase activity is altered in spontaneously hypertensive stroke-prone rats compared with spontaneously hypertensive or Wistar-Kyoto rats. Methods A colony of spontaneously hypertensive strokeprone rats was bred, in which the rate of neurological events under salt load was assessed. In a separate cohort of animals brain nitric oxide synthase activity was measured in spontaneously hypertensive stroke-prone rats (n=6) and in spontaneously hypertensive (n=6) and genetically related Wistar-Kyoto rats (n=6). Calcium dependency of nitric oxide synthase was also assessed in cortical brain samples from the three rat strains to determine if altered calcium-dependent activation of nitric oxide synthase was present. Results Brain nitric oxide synthase activity was highest in the cerebellum (eg, spontaneously hypertensive stroke-prone rats: Cerebral cortex, 10.6 ± 0.9; cerebellum, 50.1 ± 12.0; brain stem, 14.7±10.3 pmol/mg protein per minute); however, there was no difference among the three rat strains in any region (eg, cerebral cortex: Spontaneously hypertensive stroke-prone, 10.6 ± 0.9; spontaneously hypertensive, 10.8 ±0.5; Wistar-Kyoto, 10.9 ± 0.7 pmol/mg protein per minute) or at any calcium concentration tested. Conclusions A genetic defect of brain nitric oxide synthase is unlikely to be the cause of stroke predisposition in spontaneously hypertensive stroke-prone rats.

AB - Background and Purpose Nitric oxide-mediated cerebral vasodilation is altered in spontaneously hypertensive stroke-prone rats. Stroke predisposition in this strain could be related to a genetic defect of brain nitric oxide synthase, the enzyme responsible for nitric oxide production. We tested the hypothesis that brain nitric oxide synthase activity is altered in spontaneously hypertensive stroke-prone rats compared with spontaneously hypertensive or Wistar-Kyoto rats. Methods A colony of spontaneously hypertensive strokeprone rats was bred, in which the rate of neurological events under salt load was assessed. In a separate cohort of animals brain nitric oxide synthase activity was measured in spontaneously hypertensive stroke-prone rats (n=6) and in spontaneously hypertensive (n=6) and genetically related Wistar-Kyoto rats (n=6). Calcium dependency of nitric oxide synthase was also assessed in cortical brain samples from the three rat strains to determine if altered calcium-dependent activation of nitric oxide synthase was present. Results Brain nitric oxide synthase activity was highest in the cerebellum (eg, spontaneously hypertensive stroke-prone rats: Cerebral cortex, 10.6 ± 0.9; cerebellum, 50.1 ± 12.0; brain stem, 14.7±10.3 pmol/mg protein per minute); however, there was no difference among the three rat strains in any region (eg, cerebral cortex: Spontaneously hypertensive stroke-prone, 10.6 ± 0.9; spontaneously hypertensive, 10.8 ±0.5; Wistar-Kyoto, 10.9 ± 0.7 pmol/mg protein per minute) or at any calcium concentration tested. Conclusions A genetic defect of brain nitric oxide synthase is unlikely to be the cause of stroke predisposition in spontaneously hypertensive stroke-prone rats.

KW - Cerebral ischemia

KW - Focal

KW - Genetics

KW - Nitric oxide

KW - Rats

UR - http://www.scopus.com/inward/record.url?scp=0027934938&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027934938&partnerID=8YFLogxK

M3 - Article

C2 - 7518973

AN - SCOPUS:0027934938

VL - 25

SP - 1674

EP - 1677

JO - Stroke

JF - Stroke

SN - 0039-2499

IS - 8

ER -