Evidence for a role for a uterine renin-angiotensin system in decidualization in rats

Squires, P. M.; Kennedy, T. G.

doi:10.1530/jrf.0.0950791

Cited by 34 publications

(27 citation statements)

References 31 publications

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“…Several classes of potent and specific nonpeptide inhibitors have been synthesized in an effort to produce active ACE inhibitors that could be useful as antihypertensive agents (34). Captopril is thought to bind the active site of ACE in a manner analogous to endogenous substrates, and has been widely used in experiments designed to define the biological function of ACE (35)(36)(37)(38). The addition of captopril to the perfusate did not inhibit hCG-induced ovulation, despite significant reductions in both the intrafollicular Ang II content and the secretion rate ofAng II in ovaries perfused with hCG.…”

Section: Resultsmentioning

confidence: 99%

“…It has been reported that the treatment ofcultured endometrial decidual cells with enalaprilat, an another ACE inhibitor, inhibits the production of PGE2 in a dose-dependent manner, but that the concurrent administration of Ang II does not reverse the inhibitory effect of enalaprilat (38) (45)(46)(47). Our previous study also revealed that bradykinin significantly stimulated the production of PG by perfused rabbit ovaries (40).…”

Section: Resultsmentioning

confidence: 99%

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Gonadotropin stimulates ovarian renin-angiotensin system in the rabbit.

Yoshimura¹,

Koyama²,

Karube³

et al. 1994

J. Clin. Invest.

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The present study was undertaken to assess the role of ovarian renin-angiotensin system (RAS) in the preovulatory cascade induced by gonadotropin exposure. In the in vitro perfused rabbit ovaries, exposure to human chorionic gonadotropin (hCG) enhanced the secretion rate of angiotensin II (Ang II) within 1 h. The secretion rate reached maximal levels at 6 h and then declined thereafter. The intrafollicular Ang II content and renin-like activity were also significantly increased at 2 and 4 h after exposure to hCG, compared with control ovaries perfused with medium alone. The level of intrafollicular Ang II after hCG exposure significantly exceeded the concentration of Ang II in an equivalent volume of plasma. The addition of 1 ,uM captopril to the perfusate significantly inhibited the secretion rate of Ang II stimulated by hCG; however, captopril affected neither the ovulatory efficiency nor prostaglandin production in ovaries treated with hCG. Captopril significantly inhibited the resumption of meiosis in the ovulated ova and follicular oocytes stimulated by hCG. The administration of 100 ,ug Ang II at 2-h intervals to the perfusate reversed the inhibitory effects of captopril on hCG-induced oocyte maturation. In conclusion, these data indicate that gonadotropin stimulates renin-like activity and Ang11 production in the rabbit ovary. Ovarian renin-angiotensin system may play an important role in the process of oocyte maturation after exposure to gonadotropin. (J.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Gonadotropin stimulates ovarian renin-angiotensin system in the rabbit.

Yoshimura¹,

Koyama²,

Karube³

et al. 1994

J. Clin. Invest.

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show abstract

“…The synthase localized to granulosa cell surface membranes has been shown to be induced by hCG [30]. Angiotensin II is known to stimulate PG synthesis in both central and peripheral tissues by the activation of specific phospholipases [27,[31][32][33]. The activation of phospholipase C results in the production of inositol 1,4,5-triphosphate, which could release arachidonic acid for PG synthesis [34].…”

Section: Discussionmentioning

confidence: 99%

Involvement of Angiotensin II in the Process of Gonadotropin-lnduced Ovulation in Rabbits

Kuji

Sueoka

Miyazaki

et al. 1996

Biology of Reproduction

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In the present study we investigated the role of angiotensin II (Ang II) receptor subtypes in gonadotropin-induced ovulation, oocyte maturation, and ovarian steroidogenesis and prostaglandin (PG) production in in vitro-perfused rabbit ovaries. The addition to the perfusate of PD123319, a nonpeptide Ang II antagonist with a high affinity for AT2 receptors, inhibited hCG-induced ovulation in a dose-dependent manner, whereas CV-11974, a nonpeptide AT1 receptor antagonist, had no effect. The majority of ovulated ova and follicular oocytes resumed meiotic maturation in response to hCG; and PD123319, but not CV-11974, significantly inhibited hCG-induced oocyte maturation. The addition of both Ang II receptor antagonists to the perfusate had no significant effect on the concentration of progesterone in the perfusate of hCG-treated ovaries, whereas PD123319 inhibited the hCG-stimulated production of estradiol. The production of PGE2 and PGF2 alpha was significantly increased at 6 h in hCG-treated ovaries compared with ovaries before hCG administration. PD123319 inhibited the hCG-stimulated production of PGs by perfused rabbit ovaries in a dose-dependent manner, indicating that hCG-induced PG synthesis is mediated, at least in part, via the activation of AT2 receptors. Ovulatory efficiency in ovaries perfused with or without PD123319 in the presence of hCG was significantly correlated with PG production by perfused rabbit ovaries 12 h after exposure to hCG (r = 0.6553 for PGE2, p < 0.001; r = 0.4758 for PGF2 alpha, p < 0.05). In conclusion, Ang II exerts complex and coordinated control on at least two distinct aspects in the normal ovulatory process, ovulation and oocyte maturation. Ang II produced locally by gonadotropin exposure may be a part of a novel intraovarian paracrine or autocrine control mechanism that operates via the AT2 receptor in the ovary.

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“…Tenascin is expressed in the smooth muscle layers of arteries, especially during tissue remodelling processes, and is thought to be stimulated by an increase in mechanical stress or by angiotensin II [30,31]. Using enalaprilat (Merck Frosst Canada Inc., Dorval, PQ, Canada), a specific inhibitor of angiotensin-converting enzyme, Squires and Kennedy [32] provided evidence of a requirement for angiotensin II locally during the decidual cell reaction in rats.…”

Section: Discussionmentioning

confidence: 99%

Tenascin in Pregnant and Non-Pregnant Rat Uterus: Unique Spatio-Temporal Expression during Decidualization1

Michie

Head

1994

Biology of Reproduction

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Tenascin is a large extracellular matrix (ECM) protein generally restricted to developing embryonic tissues and tissues undergoing remodelling in the adult, but it has been suggested that tenascin is immunomodulatory. In this study we have used indirect immunofluorescence to investigate the distribution of tenascin within the uteri of pregnant and non-pregnant rats. The non-pregnant uterus expressed tenascin in the stroma around the glands, but only the subluminal stroma showed cyclical variations. Dependence of the latter on progesterone was verified in ovariectomized animals supplemented with steroid hormones. During early pregnancy, the uterine circular smooth muscle maintained an intense expression of tenascin. In the decidualizing endometrium, tenascin expression showed dramatic changes that reflected the regionalization of the decidualization process. On Day 6 (blastocyst attachment), tenascin immunoreactivity was prominent in the primary decidualization zone immediately surrounding the conceptus. On Day 7, expression had increased within the secondary decidua that had developed throughout the antimesometrial endometrium. By Day 8, the antimesometrial decidua showed diminished tenascin immunoreactivity; expression became largely confined to the ECM of the developing decidua in the mesometrial region, where levels were high. On Day 10, the well-developed mesometrial decidua was negative. Interestingly, tenascin expression was up-regulated in the walls of the vessels in the metrial gland within the mesometrial triangle beginning on Day 10 of pregnancy. From these studies we conclude that tenascin expression may be an important reflection of the dynamics involved with tissue restructuring during early pregnancy and may play a role in immunomodulation, since expression of this protein in the mesometrial decidua coincides with the presence of differentiating natural killer cell lineage lymphocytes in the same region.

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Evidence for a role for a uterine renin-angiotensin system in decidualization in rats

Cited by 34 publications

References 31 publications

Gonadotropin stimulates ovarian renin-angiotensin system in the rabbit.

Gonadotropin stimulates ovarian renin-angiotensin system in the rabbit.

Involvement of Angiotensin II in the Process of Gonadotropin-lnduced Ovulation in Rabbits

Tenascin in Pregnant and Non-Pregnant Rat Uterus: Unique Spatio-Temporal Expression during Decidualization1

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