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[ subject:"Physiology." ]
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The effects of hypertension on neuro...
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Iddings, Jennifer Ann.
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The effects of hypertension on neurovascular unit function and structure.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
The effects of hypertension on neurovascular unit function and structure./
作者:
Iddings, Jennifer Ann.
面頁冊數:
136 p.
附註:
Source: Dissertation Abstracts International, Volume: 76-09(E), Section: B.
Contained By:
Dissertation Abstracts International76-09B(E).
標題:
Physiology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3662851
ISBN:
9781321744828
The effects of hypertension on neurovascular unit function and structure.
Iddings, Jennifer Ann.
The effects of hypertension on neurovascular unit function and structure.
- 136 p.
Source: Dissertation Abstracts International, Volume: 76-09(E), Section: B.
Thesis (Ph.D.)--Georgia Regents University, 2015.
This item must not be sold to any third party vendors.
Functional hyperemia is the regional increase in cerebral blood flow upon increases in neuronal activity which ensures that the metabolic demands of the neurons are met. Hypertension is known to impair the hyperemic response; however, the neurovascular coupling mechanisms by which this cerebrovascular dysfunction occurs have yet to be fully elucidated. The goal of this dissertation project was to test the central hypothesis that hypertension-induced impairments in functional hyperemia are mediated by a specific disruption of communication within the neurovascular unit at the parenchymal arteriole level of the cerebrovascular tree. To test our hypothesis, we measured parenchymal arteriole reactivity, vascular smooth muscle cell Ca2+ dynamics, parenchymal arteriole remodeling and cerebral vascular density in cortical brain slices from normotensive (WKY) and hypertensive (SHR) rats. We found that vasoconstriction in response to the thromboxane A2 receptor agonist U46619 and basal vascular smooth muscle cell Ca2+ oscillation frequency were increased in parenchymal arterioles from SHR. In perfused and pressurized parenchymal arterioles, myogenic tone was increased in SHR. While K+-induced parenchymal arteriole dilations were similar in WKY and SHR, metabotropic glutamate receptor activation-induced parenchymal arteriole dilations were enhanced in SHR. Further, neuronal stimulation-evoked parenchymal arteriole dilations were similar in SHR and WKY. Parenchymal arteriole wall to lumen ratio and wall thickness were increased in SHR. Vascular density was also increased in deeper cortical layers in SHR. Our data indicate that although SHR parenchymal arterioles display vascular remodeling, neurovascular coupling is not impaired in SHR, at least at the parenchymal arteriole level.
ISBN: 9781321744828Subjects--Topical Terms:
518431
Physiology.
The effects of hypertension on neurovascular unit function and structure.
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Functional hyperemia is the regional increase in cerebral blood flow upon increases in neuronal activity which ensures that the metabolic demands of the neurons are met. Hypertension is known to impair the hyperemic response; however, the neurovascular coupling mechanisms by which this cerebrovascular dysfunction occurs have yet to be fully elucidated. The goal of this dissertation project was to test the central hypothesis that hypertension-induced impairments in functional hyperemia are mediated by a specific disruption of communication within the neurovascular unit at the parenchymal arteriole level of the cerebrovascular tree. To test our hypothesis, we measured parenchymal arteriole reactivity, vascular smooth muscle cell Ca2+ dynamics, parenchymal arteriole remodeling and cerebral vascular density in cortical brain slices from normotensive (WKY) and hypertensive (SHR) rats. We found that vasoconstriction in response to the thromboxane A2 receptor agonist U46619 and basal vascular smooth muscle cell Ca2+ oscillation frequency were increased in parenchymal arterioles from SHR. In perfused and pressurized parenchymal arterioles, myogenic tone was increased in SHR. While K+-induced parenchymal arteriole dilations were similar in WKY and SHR, metabotropic glutamate receptor activation-induced parenchymal arteriole dilations were enhanced in SHR. Further, neuronal stimulation-evoked parenchymal arteriole dilations were similar in SHR and WKY. Parenchymal arteriole wall to lumen ratio and wall thickness were increased in SHR. Vascular density was also increased in deeper cortical layers in SHR. Our data indicate that although SHR parenchymal arterioles display vascular remodeling, neurovascular coupling is not impaired in SHR, at least at the parenchymal arteriole level.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3662851
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