The Role of Angiotensin-Converting Enzyme in Blood Pressure Control, Renal Function, and Male Fertility

Esther, Charles R.; Marino, Elaine M.; Bernstein, Kenneth E.

doi:10.1016/s1043-2760(97)00039-8

Cited by 196 publications

(275 citation statements)

References 54 publications

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“…Another phenotype observed in the Ren1cϪ/Ϫ mice is medial thickening of the small arteries in the kidney but not of the vessels outside the kidney. This phenotype has been described by others in renin-deficient mice (5) as well as in mice deficient of Agt (15,17,28), Ace (18,19), Agtr1a (29), and Agtr1a/1b (20,21). Mononuclear cell infiltration surrounding the thickened arteries is evident, suggesting that some common pathogenic mechanism causes vascular thickening and perivascular inflammation.…”

Section: Discussionsupporting

confidence: 64%

Ren1c Homozygous Null Mice Are Hypotensive and Polyuric, but Heterozygotes Are Indistinguishable from Wild-Type

Takahashi¹,

López²,

Cowhig³

et al. 2005

Journal of the American Society of Nephrology

134

135

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Section: Discussionsupporting

confidence: 64%

Ren1c Homozygous Null Mice Are Hypotensive and Polyuric, but Heterozygotes Are Indistinguishable from Wild-Type

Takahashi¹,

López²,

Cowhig³

et al. 2005

Journal of the American Society of Nephrology

134

135

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“…Targeted null mutations of genes of the major components of the RAS such as angiotensinogen (Agt) (Kim et al 1995), renin (Yanai et al 2000;Chen et al 2007), angiotensin-converting enzyme (ACE) Esther Jr. et al 1996), and AT 1 receptors (Ito et al 1995;Sugaya et al 1995;Matsusaka et al 1996;Oliverio et al 1998a,b;Tsuchida et al 1998) result in reduced blood pressure and abnormal renal vascular and tubular structures. AT 1A 2/2 mice have reduced blood pressure, slight papillary hypoplasia, hyperplasia of renin-producing granular cells (Ito et al 1995;Oliverio et al 1998b;Tsuchida et al 1998), and significantly dilated efferent arterioles (Harrison-Bernard et al 2003,2006.…”

mentioning

confidence: 99%

Augmented Renal Vascular nNOS and Renin Protein Expression in Angiotensin Type 1 Receptor Null Mice

Park

Harrison‐Bernard

2007

J Histochem Cytochem.

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S U M M A R Y The present study was performed to determine the influence of absence of angiotensin type 1A (AT 1A ) and/or AT 1B receptor feedback regulation of kidney neuronal nitric oxide synthase (nNOS) and renin protein expression. Kidneys were harvested from wildtype (WT), AT 1A 2/2 , AT 1B 2/2 , and AT 1A 2/2 AT 1B 2/2 mice and immunostained for nNOS and renin protein localization. AT 1A 2/2 and AT 1A 2/2 AT 1B2/2 kidneys demonstrated an increase in the percentage of glomeruli with nNOS-positive afferent and interlobular arterioles compared with WT mice. Density of vascular nNOS immunostaining was 20-fold higher in kidneys of AT 1A 2/2 and AT 1A 2/2 AT 1B 2/2 compared with WT mice. Density of macula densa nNOS immunostaining was 7-fold higher in AT 1A 2/2 AT 1B 2/2 than in WT mice. Percent of glomeruli positive for juxtaglomerular (JG) cell renin was 3-fold higher, whereas the density of JG cell renin immunostaining was 15-fold higher in kidneys of AT 1A 2/2 and AT 1A 2/2 AT 1B 2/2 compared with WT mice. Kidneys of AT 1A 2/2 and AT 1A 2/2 AT 1B 2/2 mice displayed recruitment of renin protein expression along afferent and interlobular arterioles. Absence of AT 1 receptor signaling resulted in enhanced nNOS protein expression in both microvascular and tubular structures. Enhanced NO generation may contribute to the reduced renal vascular tone and blood pressure observed with blockade of the renin-angiotensin system.

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“…The knockout of Fkbp6 in mice as well as the identification of a functional deletion in Fkbp6 in the rat provided direct evidence for the involvement of the gene in spermatogenesis, making it an interesting candidate for the study of its involvement in male infertility in humans. [Esther et al 1996] [Liao and Roy 2002] ACT Reduced sperm count and abnormal morphology [Kotaja et al 2004] [Christensen et al 2006b] AR Pachytene spermatocyte arrest [Yeh et al 2002] [ Komori et al 1999] BCL2L2…”

Section: Fkbp6 Knockout Mouse Modelmentioning

confidence: 99%

The Use of Transgenic Mouse Models in the Study of Male Infertility

Tamowski

Aston

Carrell

2010

Systems Biology in Reproductive Medicine

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Over the past few decades with the rapid advances in embryo and embryonic stem cell manipulation techniques, transgenic mouse models have emerged as a powerful tool for the study of gene function and complex diseases including male infertility. In this review we give a brief history of the development of tools for the production of transgenic mouse models. This spans the advances from early pronuclear injection to the use of targeted embryonic stem cells to produce gene targeted, conditional, and inducible knockout mouse models. Lastly we provide a few examples to illustrate the utility of mouse models in the study of male infertility.

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The Role of Angiotensin-Converting Enzyme in Blood Pressure Control, Renal Function, and Male Fertility

Cited by 196 publications

References 54 publications

Ren1c Homozygous Null Mice Are Hypotensive and Polyuric, but Heterozygotes Are Indistinguishable from Wild-Type

Ren1c Homozygous Null Mice Are Hypotensive and Polyuric, but Heterozygotes Are Indistinguishable from Wild-Type

Augmented Renal Vascular nNOS and Renin Protein Expression in Angiotensin Type 1 Receptor Null Mice

The Use of Transgenic Mouse Models in the Study of Male Infertility

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