Brain BDNF levels are dependent on cerebrovascular endothelium-derived nitric oxide

2016 ◽  
Vol 44 (5) ◽  
pp. 2226-2235 ◽  
Author(s):  
Hayat Banoujaafar ◽  
Alice Monnier ◽  
Nicolas Pernet ◽  
Aurore Quirié ◽  
Philippe Garnier ◽  
...  
2006 ◽  
Vol 100 (1) ◽  
pp. 318-327 ◽  
Author(s):  
Jon Andresen ◽  
Nadeem I. Shafi ◽  
Robert M. Bryan

The cerebrovascular endothelium exerts a profound influence on cerebral vessels and cerebral blood flow. This review summarizes current knowledge of various dilator and constrictor mechanisms intrinsic to the cerebrovascular endothelium. The endothelium contributes to the resting tone of cerebral arteries and arterioles by tonically releasing nitric oxide (NO•). Dilations can occur by stimulated release of NO•, endothelium-derived hyperpolarization factor, or prostanoids. During pathological conditions, the dilator influence of the endothelium can turn to that of constriction by a variety of mechanisms, including decreased NO• bioavailability and release of endothelin-1. The endothelium may participate in neurovascular coupling by conducting local dilations to upstream arteries. Further study of the cerebrovascular endothelium is critical for understanding the pathogenesis of a number of pathological conditions, including stroke, traumatic brain injury, and subarachnoid hemorrhage.


2002 ◽  
Vol 1235 ◽  
pp. 369-377
Author(s):  
Zoltán Benyó ◽  
Zsombor Lacza ◽  
Tibor Hortobágyi ◽  
Christoph Görlach ◽  
Péter Sándor ◽  
...  

1994 ◽  
Vol 14 (1) ◽  
pp. 64-69 ◽  
Author(s):  
Masahiro Kobari ◽  
Yasuo Fukuuchi ◽  
Minoru Tomita ◽  
Norio Tanahashi ◽  
Shizuko Konno ◽  
...  

The effects of intracarotidly injected endothelin (ET)-1 (0.01-3 nmol) on the local cerebral blood volume (CBV) in the parietotemporal cortex were examined by the photoelectric method in 17 anesthetized cats. CBV reflects the cumulative dimensions of the cerebral microvessels. Low doses of ET-1 (0.01 and 0.1 nmol) elicited mild but significant reductions in CBV without changes in the systemic arterial blood pressure (SABP). High doses of ET-1 (3 nmol) initially induced marked declines of CBV, which were attributable to the significant falls in SABP. CBV subsequently exhibited significant increases. The CBV increases were not secondary to the accompanying elevations of SABP, since they were unaffected by inhibition of the SABP changes after preinjection of BQ-123 (1 mg/kg), an ET antagonist specific to the ETA receptors. The CBV increases, however, were prevented by continuous administration of NG-monomethyl-L-arginine (0.35 mg/kg/min), an inhibitor of nitric oxide synthesis, plus BQ-123. We conclude that while low doses of intravascular ET-1 constrict the cerebral microvessels, high doses of ET-1 dilate the cerebral microvessels through the induction of nitric oxide probably in the cerebrovascular endothelium.


Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).


2001 ◽  
Vol 28 (5-6) ◽  
pp. 459-462
Author(s):  
Pini Orbach ◽  
Charles E Wood ◽  
Maureen Keller-Wood
Keyword(s):  

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