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The mechanism of action for angiotensin-1-7 in the rostral ventrolateral medulla in the modulation of cardiovascular sympathetic nerve activity- [electronic resource]
The mechanism of action for angiotensin-1-7 in the rostral ventrolateral medulla in the modulation of cardiovascular sympathetic nerve activity- [electronic resource]
상세정보
- 자료유형
- 학위논문(국외)
- 자관 청구기호
- 기본표목-개인명
- 표제와 책임표시사항
- The mechanism of action for angiotensin-1-7 in the rostral ventrolateral medulla in the modulation of cardiovascular sympathetic nerve activity - [electronic resource] / Bilodeau, Mark S.
- 발행, 배포, 간사 사항
- 형태사항
- 1 online resource(196 p)
- 일반주기
- Source: Dissertation Abstracts International, Volume: 78-02(E), Section: B.
- 일반주기
- Adviser: James C. Leiter.
- 학위논문주기
- Thesis (Ph.D.)--Dartmouth College, 2016.
- 요약 등 주기
- 요약Elevated sympathetic discharge from the CNS is an underlying pathogenic mechanism in neurogenic hypertension and an exacerbating factor in chronic heart failure (CHF). Current treatment of these diseases focuses on attenuation of the downstream effects of this sympathetic discharge, and often involves a complex pharmaceutical regimen. The central renin angiotensin system (RAS) plays a key role in both acute and long-term regulation of cardiovascular sympathetic tone, and the rostral ventrolateral medulla (RVLM) is the site from which most of this sympathetic discharge is propagated, making it an attractive target for therapies to treat diseases involving enhanced sympathetic discharge to the cardiovascular system. Angiotensin 1-7 (ANG-(1-7)), a derivative of angiotensin I or II, is found throughout the central nervous system, and in the RVLM the receptor for ANG-(1-7), the Mas receptor, is expressed on astrocytes. To this end, we investigated the actions of ANG-(1-7) in the RVLM.
- 요약 등 주기
- 요약We recorded mean arterial pressure (MAP) and splanchnic sympathetic nerve activity (SSNA) after focal injections of ANG-(1-7) or glutamate with and without the glutamate antagonists CNQX and D-AP5 in a quest to understand the role of, and mechanism of action for ANG-(1-7) in the RVLM. We repeated these experiments with the purinergic receptor antagonist PPADS to investigate the role of ATP as a co-transmitter with glutamate. We also injected ANG-(1-7) or glutamate in the presence of the Mas receptor antagonist A-779. Last, we examined the effect of ANG-(1-7) in the setting of CHF.
- 요약 등 주기
- 요약Unilateral injection of ANG-(1-7) into the RVLM, acting through the Mas receptor, increased SSNA and MAP, and glutamate receptor antagonists partially reduced this effect; however, ATP seems to be a co-transmitter in the ANG-(1-7) effect on BP and SSNA. To our surprise, we found that the Mas receptor antagonist A-779 injected alone elicited a significant pressor effect. We investigated this finding and showed that A-779 activates the same neurotransmitters as ANG-(1-7). We did not show an effect for ANG-(1-7) in CHF. We conclude that astrocytes in the RVLM participate in central, angiotensin-dependent regulation of blood pressure and sympathetic nerve activity by activating glutamatergic and purinergic pathways.
- 주제명부출표목-일반주제명
- 부출표목-단체명
- 기본자료저록
- Dissertation Abstracts International. 78-02B(E).
- 기본자료저록
- Dissertation Abstract International
- 전자적 위치 및 접속
- 원문정보보기
- 소장사항
-
20170404 2017
MARC
008170601s2016 us esm 001c eng■001MOKWON01252796
■00520170418115120
■007cr
■020 ▼a9781339997148
■035 ▼a(MiAaPQ)AAI10144594
■040 ▼aMiAaPQ▼cMiAaPQ
■090 ▼a전자도서(박사논문)
■1001 ▼aBilodeau, Mark S.
■24514▼aThe mechanism of action for angiotensin-1-7 in the rostral ventrolateral medulla in the modulation of cardiovascular sympathetic nerve activity▼h[electronic resource]▼cBilodeau, Mark S.
■260 ▼a[Sl]▼bDartmouth College▼c2016
■300 ▼a1 online resource(196 p)
■500 ▼aSource: Dissertation Abstracts International, Volume: 78-02(E), Section: B.
■500 ▼aAdviser: James C. Leiter.
■5021 ▼aThesis (Ph.D.)--Dartmouth College, 2016.
■520 ▼aElevated sympathetic discharge from the CNS is an underlying pathogenic mechanism in neurogenic hypertension and an exacerbating factor in chronic heart failure (CHF). Current treatment of these diseases focuses on attenuation of the downstream effects of this sympathetic discharge, and often involves a complex pharmaceutical regimen. The central renin angiotensin system (RAS) plays a key role in both acute and long-term regulation of cardiovascular sympathetic tone, and the rostral ventrolateral medulla (RVLM) is the site from which most of this sympathetic discharge is propagated, making it an attractive target for therapies to treat diseases involving enhanced sympathetic discharge to the cardiovascular system. Angiotensin 1-7 (ANG-(1-7)), a derivative of angiotensin I or II, is found throughout the central nervous system, and in the RVLM the receptor for ANG-(1-7), the Mas receptor, is expressed on astrocytes. To this end, we investigated the actions of ANG-(1-7) in the RVLM.
■520 ▼aWe recorded mean arterial pressure (MAP) and splanchnic sympathetic nerve activity (SSNA) after focal injections of ANG-(1-7) or glutamate with and without the glutamate antagonists CNQX and D-AP5 in a quest to understand the role of, and mechanism of action for ANG-(1-7) in the RVLM. We repeated these experiments with the purinergic receptor antagonist PPADS to investigate the role of ATP as a co-transmitter with glutamate. We also injected ANG-(1-7) or glutamate in the presence of the Mas receptor antagonist A-779. Last, we examined the effect of ANG-(1-7) in the setting of CHF.
■520 ▼aUnilateral injection of ANG-(1-7) into the RVLM, acting through the Mas receptor, increased SSNA and MAP, and glutamate receptor antagonists partially reduced this effect; however, ATP seems to be a co-transmitter in the ANG-(1-7) effect on BP and SSNA. To our surprise, we found that the Mas receptor antagonist A-779 injected alone elicited a significant pressor effect. We investigated this finding and showed that A-779 activates the same neurotransmitters as ANG-(1-7). We did not show an effect for ANG-(1-7) in CHF. We conclude that astrocytes in the RVLM participate in central, angiotensin-dependent regulation of blood pressure and sympathetic nerve activity by activating glutamatergic and purinergic pathways.
■590 ▼aSchool code: 0059.
■650 4▼aPhysiology
■690 ▼a0719
■71020▼aDartmouth College▼bExperimental and Molecular Medicine.
■7730 ▼tDissertation Abstracts International▼g78-02B(E).
■773 ▼tDissertation Abstract International
■790 ▼a0059
■791 ▼aPh.D.
■792 ▼a2016
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T14488655▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
■980 ▼a20170404▼f2017
