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Flow‐induced Constriction of Cerebral Arteries in Hypertension: a Protective Mechanism Against Stroke?
Author(s) -
Szarka Nikolett,
Toth Peter,
Koller Akos
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.832.5
Subject(s) - constriction , medicine , cerebral arteries , stroke (engine) , cerebral circulation , cardiology , cerebral blood flow , anesthesia , intracerebral hemorrhage , middle cerebral artery , ischemia , mechanical engineering , subarachnoid hemorrhage , engineering
Objective. Intracerebral hemorrhage (ICH) is the most fatal stroke subtype. The pressure‐induced constriction of cerebral arteries is enhanced in hypertension protecting the cerebral circulation, but this response is lost before ICH in stroke‐prone spontaneously hypertensive rats (spSHR). We have shown that flow‐induced constriction of cerebral arteries regulates cerebrovascular resistance in addition to myogenic response. Thus, we hypothesized that flow‐induced constriction is increased in hypertension and the enhanced response is lost before ICH. Methods. Middle cerebral arteries (MCA) isolated from SHR and spSHR (control: Wystar‐Kyoto) were transferred into an isolated‐vessel‐chamber and responses were obtained to increases in flow at age of 9. weeks and on the 13. weeks before and after the neurological signs of stroke. Results. Flow‐induced constriction was enhanced in SHR, but it was decreased in SHRsp at 9. weeks and virtually absent at the 13. weeks before the onset of stroke. The differences in the magnitude of the flow‐induced responses between the groups were diminished by inhibition of the production of the constrictor 20‐HETE. Conclusions Increased 20‐HETE‐mediated flow‐induced arterial constriction may be another local mechanism protecting against the development of ICH in hypertension. Support: Hungarian Natl Sci Res Fund (OTKA) K 108444, European Union's Seventh Framework Programme, No. 606998.