Is Ouabain Produced by the Adrenal Gland?

Foster, Richard H.; Prat, Hernán; Rothman, Ilan

doi:10.1016/s0306-3623(98)00021-4

Cited by 4 publications

(2 citation statements)

References 39 publications

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“…The AT 2 receptor promoter does not contain estrogen response elements [48]. Estrogen may activate AT 2 receptor transcription from alternative response elements such as the activator protein site (AP-1) [49, 50], by increased intracellular sodium concentration through estrogen inhibition of Na + ,K + -ATPase [51, 52], a ouabain-sensitive mechanism [53] or by receptor activation potentiating its own expression, because AT 2 receptors stimulate endogenous adrenal ouabain, and this inhibits Na + ,K + -ATPase [54]. …”

Section: Discussionmentioning

confidence: 99%

Estrogen Reduces Aldosterone, Upregulates Adrenal Angiotensin II AT<sub>2</sub> Receptors and Normalizes Adrenomedullary Fra-2 in Ovariectomized Rats

Macova¹,

Armando²,

Zhou³

et al. 2008

Neuroendocrinology

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We studied the effect of ovariectomy and estrogen replacement on expression of adrenal angiotensin II AT₁ and AT₂ receptors, aldosterone content, catecholamine synthesis, and the transcription factor Fos-related antigen 2 (Fra-2). Ovariectomy increased AT₁ receptor expression in the adrenal zona glomerulosa and medulla, and decreased adrenomedullary catecholamine content and Fra-2 expression when compared to intact female rats. In the zona glomerulosa, estrogen replacement normalized AT₁ receptor expression, decreased AT_1B receptor mRNA, and increased AT₂ receptor expression and mRNA. Estrogen treatment decreased adrenal aldosterone content. In the adrenal medulla, the effects of estrogen replacement were: normalized AT₁ receptor expression, increased AT₂ receptor expression, AT₂ receptor mRNA, and tyrosine hydroxylase mRNA, and normalized Fra-2 expression and catecholamine content. We demonstrate that the constitutive adrenal expression of AT₁ receptors, catecholamine synthesis and Fra-2 expression are partially under the control of reproductive hormones. Our results suggest that estrogen treatment decreases aldosterone production through AT₁ receptor downregulation and AT₂ receptor upregulation. AT₂ receptor upregulation and modulation of Fra-2 expression may participate in the estrogen-dependent normalization of adrenomedullary catecholamine synthesis in ovariectomized rats. The AT₂ receptor upregulation and the decrease in AT₁ receptor function and in the production of the fluid-retentive, pro-inflammatory hormone aldosterone partially explain the protective effects of estrogen therapy.

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Section: Discussionmentioning

confidence: 99%

Estrogen Reduces Aldosterone, Upregulates Adrenal Angiotensin II AT<sub>2</sub> Receptors and Normalizes Adrenomedullary Fra-2 in Ovariectomized Rats

Macova¹,

Armando²,

Zhou³

et al. 2008

Neuroendocrinology

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“…Interestingly, endogenous ouabain has also been identified [14] and its plasmatic concentration ranges from 50 pM to 80 nM [13,15,16]. It is synthesized and released by adrenal glands [17] and it was demonstrated that ACTH is one of the stimuli for its release [14]. It is important to emphasize that not only adrenal glands synthesize ouabain.…”

Section: Introductionmentioning

confidence: 99%

The Trophic Effect of Ouabain on Retinal Ganglion Cell is Mediated by EGF Receptor and PKC δ Activation

et al. 2010

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It was already shown that ouabain treatment can stimulate PKC isoenzymes leading to the activation of intracellular pathways involved in cell survival, growth and proliferation. We have previously demonstrated that ouabain or PMA treatment increases retinal ganglion cell survival, an effect mediated by PKC activation. The aim of this work was to investigate the role of EGF receptors in the ouabain effect and also to study which PKC isoform is activated by treatment with ouabain and PMA. Our results show that 2.5 microM tyrphostin, 1.0 microM PP1, 4.0 microM U73122, 1.0 microM JNK inhibitor V and 2.0 microM rottlerin blocked the ouabain effect indicating an involvement of receptors for EGF, Src, PLC, JNK and PKC delta respectively. The effect of PMA was only abolished when cultures were treated with rottlerin or with the JNK inhibitor suggesting the involvement of PKC delta and JNK. These results indicate that PKC delta could be a key regulator of retinal ganglion cell survival.

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Ouabain induces an increase of retinal ganglion cell survival in vitro: The involvement of protein kinase C

et al. 2005

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Is Ouabain Produced by the Adrenal Gland?

Cited by 4 publications

References 39 publications

Estrogen Reduces Aldosterone, Upregulates Adrenal Angiotensin II AT<sub>2</sub> Receptors and Normalizes Adrenomedullary Fra-2 in Ovariectomized Rats

Estrogen Reduces Aldosterone, Upregulates Adrenal Angiotensin II AT<sub>2</sub> Receptors and Normalizes Adrenomedullary Fra-2 in Ovariectomized Rats

The Trophic Effect of Ouabain on Retinal Ganglion Cell is Mediated by EGF Receptor and PKC δ Activation

Ouabain induces an increase of retinal ganglion cell survival in vitro: The involvement of protein kinase C

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