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.
- Cerebral ischemia
- Nitric oxide
ASJC Scopus subject areas
- Clinical Neurology
- Cardiology and Cardiovascular Medicine
- Advanced and Specialized Nursing