The Ovarian Renin–Angiotensin System in Reproductive Physiology

Yoshimura, Yasunori

doi:10.1006/frne.1997.0152

Cited by 96 publications

(95 citation statements)

References 223 publications

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“…There is also considerable evidence for the existence of local RASs in reproductive tissues such as the uterus (Ryan & Johnson 1969), testis (Pandey et al 1984) and placenta (Hodari et al 1967, Skinner et al 1968. With regard to the ovary, components of the RAS have been identified in many species, and locally produced ANG II has been suggested to have diverse roles including the modulation of atresia, steroidogenesis, ovulation, oocyte maturation, corpus luteum formation and angiogenesis (Yoshimura 1997, Speth et al 1999, Vinson et al 1999. However, some of the actions of ANG II appear contradictory, and as the distribution, abundance and role of the ovarian RAS varies between species, further investigation into the ovarian RAS is justified.…”

Section: Introductionmentioning

confidence: 99%

“…While studies of the rat ovary have provided information regarding the local effects of ANG II (Yoshimura 1997, Speth et al 1999, Vinson et al 1999, the characterisation of the rat ovarian RAS has to some extent been limited by the low levels of tissue RAS expression (Phillips et al 1993). The normal Sprague-Dawley (SD) rat possesses the Ren-1 gene which is responsible for the expression of renin in kidney and low levels of renin in extra-renal tissues (Ekker et al 1989).…”

Section: Introductionmentioning

confidence: 99%

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Angiotensin II influences ovarian follicle development in the transgenic (mRen-2)27 and Sprague-Dawley rat

Gooyer¹,

Skinner²,

Wlodek³

et al. 2004

Journal of Endocrinology

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There is accumulating evidence that local reninangiotensin systems (RASs) influence cell growth and organ function in a variety of tissues including the ovary. The first aim of this study was to characterise the cellular location of RAS components in the rat ovary. This was facilitated by the use of the hypertensive transgenic (mRen-2)27 rat which overexpresses renin and angiotensin in extra-renal tissues. Comparisons were made with normal Sprague-Dawley (SD) rats. The second aim was to determine if the upregulated RAS of the transgenic (mRen-2)27 rat and infusion of angiotensin II (ANG II) in SD rats influences follicle number and litter size. Gene expression, immunohistochemical and autoradiographic techniques were used to identify a discrete RAS including ANG II receptors in the ovarian stroma, follicles (particularly atretic) and to a lesser extent corpora lutea. The RAS at these sites was most abundant in homozygous (HMZ) followed by heterozygous (HTZ) (mRen-2)27 rats and then SD rats. Large antral and preovulatory follicles and litter size were reduced in (mRen-2)27 rats. In HMZ (mRen-2)27 rats and SD rats infused with ANG II, angiotensin 1a (AT 1a ) receptor mRNA in the ovarian stroma was lower than control SD rats and was associated with a reduction in large antral and preovulatory follicles. These findings indicate that upregulation of the ovarian RAS in the rat influences follicular development and, potentially, reproductive capacity.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Angiotensin II influences ovarian follicle development in the transgenic (mRen-2)27 and Sprague-Dawley rat

Gooyer¹,

Skinner²,

Wlodek³

et al. 2004

Journal of Endocrinology

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Section: Rklk3);mentioning

confidence: 99%

“…Angiotensin is believed to play numerous roles in the pre-and postovulatory follicle, including vascularisation of the early follicle, maturation of the oocyte, and regulation of stromal, thecal, granulosa and luteal cell growth and proliferation (Andrade-Gordon et al 1991, Yoshimura 1997. As rKLK2 levels are not increased at this time, tonin may not be a physiological activator of angiotensin II in the rat ovary and thus it is possible that angiotensin is activated by other factors, such as tissue plasminogen activator in this tissue (Yoshimura 1997). The marked increase in expression of rKLK2 at 20-30 h after hCG administration may be indicative of a role for this enzyme in the process of luteolysis, particularly in the formation of the vasculature associated with the luteinised granulosa cells (Hillier 1994), although this has yet to be determined.…”

Section: Rklk3);mentioning

confidence: 99%

Kallikrein gene expression in the gonadotrophin-stimulated rat ovary

Holland

Findlay

Clements

2001

Journal of Endocrinology

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The kallikreins (KLKs) are a highly conserved multi-gene family of serine proteases that are expressed in a wide variety of tissues and act on a diverse range of substrates. KLK-like enzyme activity has variously been reported to increase or decrease during the period leading up to ovulation in the equine chorionic gonadotrophin (eCG)-primed, human chorionic gonadotrophin (hCG)-stimulated immature rat ovary. These earlier studies, which used biochemical assays to detect enzyme activity, lacked the specificity and sensitivity necessary to characterise conclusively the activity of the individual KLK gene family members. In this study, we have used a gene-specific RT-PCR/Southern hybridisation strategy to delineate the expression patterns of six of the individual KLK genes expressed in the rat ovary (rKLK1-3 and rKLK7-9). We have identified three broad patterns of expression in the eCG/hCG-stimulated ovary in which there is either a post-eCG increase/pre-ovulatory decrease in rKLK expression (rKLK1, rKLK3), a peri-ovulatory decrease in expression (rKLK2, rKLK8) or a relatively unchanged pattern of expression (rKLK7, rKLK9). In addition to clarifying the earlier biochemical studies, these findings support a differential role for the individual KLKs in the ovulatory process.

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“…Nas últimas décadas, uma série de fatores de crescimento e peptídeos regulatórios foram identificados como reguladores do crescimento folicular, ovulação e luteinização (YOSHIMURA, 1997;RICHARDS et al, 2002). Nesse sentido, alguns modelos de sinalização para o desencadeamento da ovulação têm sido propostos para mamíferos, a partir do pico ovulatório de gonadotrofina (BRIDGES et al, 2006;FORTUNE et al, 2009).…”

Section: Introductionunclassified