東華大學圖書館 |

Language: English

Help

回圖書館首頁

手機版館藏查詢

Back

Switch To: Labeled | MARC Mode | ISBD

The effects of hypertension on neuro...

Iddings, Jennifer Ann.

Linked to FindBook

Google Book

Amazon

博客來

The effects of hypertension on neurovascular unit function and structure.

Record Type:	Electronic resources : Monograph/item
Title/Author:	The effects of hypertension on neurovascular unit function and structure./
Author:	Iddings, Jennifer Ann.
Description:	136 p.
Notes:	Source: Dissertation Abstracts International, Volume: 76-09(E), Section: B.
Contained By:	Dissertation Abstracts International76-09B(E).
Subject:	Physiology. -
Online resource:	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.
LDR:02940nmm a2200301 4500 001 2066462
005 20151106144902.5
008 170521s2015 ||||||||||||||||| ||eng d
020 $a 9781321744828
035 $a (MiAaPQ)AAI3662851
035 $a AAI3662851
040 $a MiAaPQ $c MiAaPQ
100 1 $a Iddings, Jennifer Ann. $3 3181260
245 1 4 $a The effects of hypertension on neurovascular unit function and structure.
300 $a 136 p.
500 $a Source: Dissertation Abstracts International, Volume: 76-09(E), Section: B.
500 $a Adviser: Jessica A. Filosa.
502 $a Thesis (Ph.D.)--Georgia Regents University, 2015.
506 $a This item must not be sold to any third party vendors.
506 $a This item must not be added to any third party search indexes.
520 $a 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.
520 $a INDEX WORDS: hypertension, functional hyperemia, neurovascular coupling, astrocyte, parenchymal arteriole, brain slice.
590 $a School code: 1749.
650 4 $a Physiology. $3 518431
690 $a 0719
710 2 $a Georgia Regents University. $3 3170760
773 0 $t Dissertation Abstracts International $g 76-09B(E).
790 $a 1749
791 $a Ph.D.
792 $a 2015
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3662851