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The role of angiotension-(1-7) in ca...

Grobe, Justin L.

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The role of angiotension-(1-7) in cardiovascular physiology.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	The role of angiotension-(1-7) in cardiovascular physiology./
作者:	Grobe, Justin L.
面頁冊數:	133 p.
附註:	Adviser: Michael J. Katovich.
Contained By:	Dissertation Abstracts International67-06B.
標題:	Biology, Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3224545
ISBN:	9780542755910

The role of angiotension-(1-7) in cardiovascular physiology.
Grobe, Justin L.

The role of angiotension-(1-7) in cardiovascular physiology. - 133 p.

Adviser: Michael J. Katovich.

Thesis (Ph.D.)--University of Florida, 2006.

Heart failure (HF) is a devastating condition that impacts our society emotionally, physiologically, and fiscally, and it is a growing problem in the United States. Aberrant activity of the renin-angiotensin hormone system (RAS) has been implicated as a causative factor in HF. Recently, a new angiotensin converting enzyme 2 (ACE2) was recognized, which catalyzes the degradation of the active angiotensin II (Ang II) hormone to angiotensin-(1-7) (Ang-(1-7)). Studies into the actions of ACE2 have led to the concept that Ang-(1-7) may act as an active, endogenous inhibitor of the RAS. Interestingly, investigations into the mechanisms of action of ACE inhibitors and AT1R antagonists have revealed that both of these treatments result in increased circulating levels of Ang-(1-7). Some have therefore hypothesized that pharmacological inhibitors of the RAS may provide cardioprotective effects through the actions of Ang-(1-7).

ISBN: 9780542755910Subjects--Topical Terms:

1017816
Biology, Physiology.

The role of angiotension-(1-7) in cardiovascular physiology.
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100 1 $a Grobe, Justin L. $3 1287122
245 1 4 $a The role of angiotension-(1-7) in cardiovascular physiology.
300 $a 133 p.
500 $a Adviser: Michael J. Katovich.
500 $a Source: Dissertation Abstracts International, Volume: 67-06, Section: B, page: 2997.
502 $a Thesis (Ph.D.)--University of Florida, 2006.
520 $a Heart failure (HF) is a devastating condition that impacts our society emotionally, physiologically, and fiscally, and it is a growing problem in the United States. Aberrant activity of the renin-angiotensin hormone system (RAS) has been implicated as a causative factor in HF. Recently, a new angiotensin converting enzyme 2 (ACE2) was recognized, which catalyzes the degradation of the active angiotensin II (Ang II) hormone to angiotensin-(1-7) (Ang-(1-7)). Studies into the actions of ACE2 have led to the concept that Ang-(1-7) may act as an active, endogenous inhibitor of the RAS. Interestingly, investigations into the mechanisms of action of ACE inhibitors and AT1R antagonists have revealed that both of these treatments result in increased circulating levels of Ang-(1-7). Some have therefore hypothesized that pharmacological inhibitors of the RAS may provide cardioprotective effects through the actions of Ang-(1-7).
520 $a The present studies were designed to characterize the cardioprotective actions of Ang-(1-7) in various models of cardiac remodeling. The protective effect of Ang-(1-7) was evaluated in Ang II-infusion, mineralocorticoid, and beta-adrenergic models of cardiac remodeling. Further, due to gender differences in the development and progression of heart failure, the protective actions of Ang-(1-7) were evaluated in intact and ovariectomized female rats. Cardiac remodeling was inhibited by Ang-(1-7), with specific effects determined by the type of stimulus, and estrogens were determined to play an important role in regulating tissue sensitivity to Ang-(1-7).
520 $a From these findings, it was concluded that Ang-(1-7) has specific actions in the cardiovascular system, some of which oppose the actions of its precursor, Ang II. In addition, our results lead us to hypothesize that estrogen replacement therapy during menopause may predispose women to cardiovascular diseases through decreased tissue sensitivity to the protective Ang-(1-7) hormone. Future studies should more directly characterize the effects of estrogens on cardiac tissue, and further elucidate the tissue-level and intracellular signaling mechanisms of Ang-(1-7). Our results indicate that Ang-(1-7) may represent a new, unexploited class of targets for pharmacological intervention before and during HF.
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