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The selective knockout of murine ang...

Cole, Justin McGraw.

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The selective knockout of murine angiotensin-converting enzyme.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	The selective knockout of murine angiotensin-converting enzyme./
Author:	Cole, Justin McGraw.
Description:	160 p.
Notes:	Adviser: Kenneth E. Bernstein.
Contained By:	Dissertation Abstracts International63-07B.
Subject:	Biology, Animal Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3058999
ISBN:	0493744541

The selective knockout of murine angiotensin-converting enzyme.
Cole, Justin McGraw.

The selective knockout of murine angiotensin-converting enzyme. - 160 p.

Adviser: Kenneth E. Bernstein.

Thesis (Ph.D.)--Emory University, 2002.

The renin-angiotensin system (RAS) plays a central role in controlling mammalian blood pressure; inhibitors of this system have found broad use in the treatment of hypertension, congestive heart failure and diabetic nephropathy. Our laboratory has characterized two strains of angiotensin-converting enzyme (ACE) knockout, one a compete null (ACE.1 strain) and one that specifically lacks tissue-bound ACE (ACE.2 strain). These animals demonstrate a complex phenotype with abnormalities in cardiovascular, renal, and electrolyte homeostasis. We have recently observed that ACE knockout mice also have a normocytic, normochromic anemia with a &sim;25% reduction in red cell mass. This anemia is associated with an elevation in plasma erythropoietin and is sensitive to the exogenous administration of angiotensin II. Because clinicians often observe reduced hematocrit with the use of ACE inhibitors, these data have implications for the management of chronically ill patients on inhibitors of the RAS. Due to the multifaceted phenotype of the ACE.1 and ACE.2 knockout mice, we were then interested in examining the role of different tissue beds of ACE in the physiologic function of the RAS. To investigate this question, we used a strategy of targeted homologous recombination to create a mouse that expresses ACE selectively in hepatocytes (ACE.3 strain). The ACE.3 −/− mouse has an 87-fold increase in hepatic ACE but does not produce ACE within the lung, the aorta, or any vascular structure. The analysis of this animal, and a compound heterozygote bearing one ACE.3 allele and one null allele, indicates the remarkable plasticity of the RAS in the control of blood pressure, renal function, and erythropoiesis.

ISBN: 0493744541Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

The selective knockout of murine angiotensin-converting enzyme.
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020 $a 0493744541
035 $a (UnM)AAI3058999
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100 1 $a Cole, Justin McGraw. $3 1251081
245 1 0 $a The selective knockout of murine angiotensin-converting enzyme.
300 $a 160 p.
500 $a Adviser: Kenneth E. Bernstein.
500 $a Source: Dissertation Abstracts International, Volume: 63-07, Section: B, page: 3092.
502 $a Thesis (Ph.D.)--Emory University, 2002.
520 $a The renin-angiotensin system (RAS) plays a central role in controlling mammalian blood pressure; inhibitors of this system have found broad use in the treatment of hypertension, congestive heart failure and diabetic nephropathy. Our laboratory has characterized two strains of angiotensin-converting enzyme (ACE) knockout, one a compete null (ACE.1 strain) and one that specifically lacks tissue-bound ACE (ACE.2 strain). These animals demonstrate a complex phenotype with abnormalities in cardiovascular, renal, and electrolyte homeostasis. We have recently observed that ACE knockout mice also have a normocytic, normochromic anemia with a &sim;25% reduction in red cell mass. This anemia is associated with an elevation in plasma erythropoietin and is sensitive to the exogenous administration of angiotensin II. Because clinicians often observe reduced hematocrit with the use of ACE inhibitors, these data have implications for the management of chronically ill patients on inhibitors of the RAS. Due to the multifaceted phenotype of the ACE.1 and ACE.2 knockout mice, we were then interested in examining the role of different tissue beds of ACE in the physiologic function of the RAS. To investigate this question, we used a strategy of targeted homologous recombination to create a mouse that expresses ACE selectively in hepatocytes (ACE.3 strain). The ACE.3 −/− mouse has an 87-fold increase in hepatic ACE but does not produce ACE within the lung, the aorta, or any vascular structure. The analysis of this animal, and a compound heterozygote bearing one ACE.3 allele and one null allele, indicates the remarkable plasticity of the RAS in the control of blood pressure, renal function, and erythropoiesis.
590 $a School code: 0665.
650 4 $a Biology, Animal Physiology. $3 1017835
650 4 $a Chemistry, Biochemistry. $3 1017722
690 $a 0433
690 $a 0487
710 2 0 $a Emory University. $3 1017429
773 0 $t Dissertation Abstracts International $g 63-07B.
790 $a 0665
790 1 0 $a Bernstein, Kenneth E., $e advisor
791 $a Ph.D.
792 $a 2002
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3058999