Nitric Oxide Synthase Inhibition in Spontaneously Hypertensive Rats

Hypertension ◽  
1995 ◽  
Vol 26 (2) ◽  
pp. 249-255 ◽  
Author(s):  
Hidehiko Ono ◽  
Yuko Ono ◽  
Edward D. Frohlich
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Oxide Synthase

Expression of endothelin receptors and nitric oxide synthase in the brain of stroke-prone spontaneously hypertensive rats with cerebral apoplexy

1997 ◽  
Vol 756 (1-2) ◽  
pp. 61-67 ◽  
Author(s):  
Yasuko Sakurai-Yamashita ◽  
Kimihiro Yamashita ◽  
Yasufumi Kataoka ◽  
Akihiko Himeno ◽  
Masami Niwa ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Spontaneously Hypertensive Rats ◽  
Endothelin Receptors ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Oxide Synthase ◽  
The Brain

scholarly journals Rapamycin Induces an eNOS (Endothelial Nitric Oxide Synthase) Dependent Increase in Brain Collateral Perfusion in Wistar and Spontaneously Hypertensive Rats

Stroke ◽  
2020 ◽  
Vol 51 (9) ◽  
pp. 2834-2843
Author(s):  
Daniel J. Beard ◽  
Zhaojin Li ◽  
Anna M. Schneider ◽  
Yvonne Couch ◽  
Marilyn J. Cipolla ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Nitric Oxide Synthase ◽  
Spontaneously Hypertensive Rats ◽  
Infarct Volume ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Background and Purpose: Rapamycin is a clinically approved mammalian target of rapamycin inhibitor that has been shown to be neuroprotective in animal models of stroke. However, the mechanism of rapamycin-induced neuroprotection is still being explored. Our aims were to determine if rapamycin improved leptomeningeal collateral perfusion, to determine if this is through eNOS (endothelial nitric oxide synthase)-mediated vessel dilation and to determine if rapamycin increases immediate postreperfusion blood flow. Methods: Wistar and spontaneously hypertensive rats (≈14 weeks old, n=22 and n=15, respectively) were subjected to ischemia by middle cerebral artery occlusion (90 and 120 minutes, respectively) with or without treatment with rapamycin at 30-minute poststroke. Changes in middle cerebral artery and collateral perfusion territories were measured by dual-site laser Doppler. Reactivity to rapamycin was studied using isolated and pressurized leptomeningeal anastomoses. Brain injury was measured histologically or with triphenyltetrazolium chloride staining. Results: In Wistar rats, rapamycin increased collateral perfusion (43±17%), increased reperfusion cerebral blood flow (16±8%) and significantly reduced infarct volume (35±6 versus 63±8 mm 3 , P <0.05). Rapamycin dilated leptomeningeal anastomoses by 80±9%, which was abolished by nitric oxide synthase inhibition. In spontaneously hypertensive rats, rapamycin increased collateral perfusion by 32±25%, reperfusion cerebral blood flow by 44±16%, without reducing acute infarct volume 2 hours postreperfusion. Reperfusion cerebral blood flow was a stronger predictor of brain damage than collateral perfusion in both Wistar and spontaneously hypertensive rats. Conclusions: Rapamycin increased collateral perfusion and reperfusion cerebral blood flow in both Wistar and comorbid spontaneously hypertensive rats that appeared to be mediated by enhancing eNOS activation. These findings suggest that rapamycin may be an effective acute therapy for increasing collateral flow and as an adjunct therapy to thrombolysis or thrombectomy to improve reperfusion blood flow.

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