Effects of estradiol on sodium and potassium balances in adrenalectomized dogs

Johnson, J. A.; Davis, JO; Brown, Peter R.; Wheeler, P G; Witty, RT

doi:10.1152/ajplegacy.1972.223.1.194

Cited by 21 publications

(5 citation statements)

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“…Ele vated All levels produce an opposite effect. Since estrogens exert a mineralocorticoid effect in addition to their effect on the renin-aldosterone system [21] it might be argued that in this study a positive sodium balance may be responsible for the observed dowm-regulation of the adrenal All recep tor via lowered circulating All (table III, All at 14 days). This does not appear to be the predominant mechanism of action since up-regulation of the mesenteric artery All re ceptor was not observed at any time period during the pres ent study.…”

Section: Discussionmentioning

confidence: 65%

Chronic Estradiol Treatment Decreases Angiotensin II Receptor Density in the Anterior Pituitary Gland and Adrenal Cortex but Not in the Mesenteric Artery

Carrière¹,

Léan²,

Gutkowska³

et al. 1986

Neuroendocrinology

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Chronic estrogen treatment has been shown to produce a marked reduction in anterior pituitary angiotensin II (AII) receptor density. In order to determine whether this effect is generalized, we studied the effect of chronic estradiol treatment on AII receptor density in the anterior pituitary gland, adrenal cortex and mesenteric artery of ovariectomized (OVX) rats. Treated rats were injected daily with 25 µg of estradiol valerate while controls received only the vehicle. Binding affinity and density of AII receptors were measured using the AII antagonist [¹²⁵I]-Sar¹Ile⁸ AII ([¹²⁵I]-SARILE). Following 7-, 14- or 28-day treatments, AII receptor density decreased by approximately 80% in the anterior pituitary; 30% in the adrenal cortex and remained the same in mesenteric artery particulate fractions. In all 3 target tissues, dissociation constants (KD) for binding of [¹²⁵I]-SARILE were in the nanomolar range and were the same between control and treated rats. Using conscious rats, estradiol treatment for 7 days was also shown to block the release of aldosterone by low dose infusions of AII (10 ng/min, 30 min). Plasma AII and plasma renin activity were also the same or slightly decreased following estradiol treatments. This study suggests that estrogens may be important modulators of the AII receptor and may be directly involved in modulating target cell responsiveness to AII as expressed through differential down-regulation of AII receptors.

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Section: Discussionmentioning

confidence: 65%

Chronic Estradiol Treatment Decreases Angiotensin II Receptor Density in the Anterior Pituitary Gland and Adrenal Cortex but Not in the Mesenteric Artery

Carrière¹,

Léan²,

Gutkowska³

et al. 1986

Neuroendocrinology

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“…Estrogen usage induced many physiological changes including alterations of vascular reactivity [Rosenfeld and Jackson, 1984;Naden and Rosenfeld, 1985;Vargas et al, 1995], sympathetic activity [Iversen, 1973] and the sodium balance [Johnson et al, 1972]. Specific binding sites of estrogen have been reported in aorta and cardiac ventricular tissues of both male and female rats [Stumpf et al, 1977;Lin and Shain, 1985].…”

mentioning

confidence: 99%

Effects of estradiol on aldosterone secretion in ovariectomized rats

Kau

Lo²,

Tsai³

et al. 1999

J. Cell. Biochem.

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The effects and action mechanisms of estradiol on aldosterone secretion in female rats were studied. Replacement of estradiol benzoate (EB) increased the levels of plasma estradiol and aldosterone in ovariectomized (Ovx) rats. The aldosterone release from zona glomerulosa (ZG) cells was higher in EB-treated rats than in oil-treated animals. EB treatment potentiated the responses of aldosterone release to adrenocorticotropic hormone (ACTH), forskolin (FSK), and 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP). Administration of EB in vivo did not alter cAMP production in response to ACTH or FSK. Although angiotensin II (Ang II) increased aldosterone secretion by rat ZG cells, the stimulatory effect of Ang II on the release of aldosterone was not altered by EB treatment. The conversions of [3H]-deoxycorticosterone to [3H]-corticosterone and [3H]-corticosterone to [3H]-aldosterone in EB-treated groups were greater than those in the oil-treated group. These results suggest that estradiol increases aldosterone secretion in part through the mechanisms involving the activation of the post-cAMP pathway, 11beta-hydroxylase and aldosterone synthase activity.

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“…All these changes were accompanied by an increase in weight in 4/6 sub¬ jects, with a return to normal of all the parameters within 4 days of cessation of oestrogen administra¬ tion. Oestrogens produce sodium and water reten¬ tion in animals even during the phase of sodium escape to mineralocorticoid (Johnson et al 1970) or in adrenalectomized animals (Johnson et al 1972) but not in hypophysectomized animals sug¬ gesting that the water retention at least was me¬ diated by vasopressin release, as has been observed in rats (Skowski et al 1979). The exact mechanism by which oestrogens modify the response of AVP release to an osmolar stimulus remains unclear.…”

Section: Discussionmentioning

confidence: 74%

Studies of the factors modulating antidiuretic hormone excretion in man in response to the osmolar stimulus: effects of oestrogen and angiotensin II

Vallotton

Gaillard

1983

Acta Endocrinologica

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The aim of this study was to assess the influence of hormones known to regulate fluid and electrolyte balance on the release of antidiuretic hormone induced by raising serum osmolality. The stimulus provoked by the infusion of a 2.5% NaCl solution induces an increase of urinary [arginine-8]-vasopressin from 1.12 to 2.64 ng/h in men and from 1.65 to 7.27 ng/h in women as has been previously reported. These results were compared to those obtained in males infused with angiotensin II (All) before and during a hypertonic sodium load and in males infused with hypertonic saline on the fourth day of administration of ethinyl-oestradiol. During the combined infusion of All and then hypertonic saline, the mean hourly urinary excretion of AVP increased from 2.8 to 5.67 ng/h. Within each group the increase of urinary AVP was highly significant. The rise of urinary AVP during All infusion was significantly different from the rise observed both in untreated males and untreated females, lying in between. The mean hourly excretion rate of AVP increased before and after hypertonic saline loading from 2.65 to 5.3 ng/h in males pre-treated with ethinyl-oestradiol. The significant difference observed between males and females is reduced when males treated with oestrogen were compared to female subjects. In each group plasma renin activity decreased to low values during the salt-loading test. During oestrogen treatment PRA and plasma renin substrate rose, while urinary aldosterone remained almost unchanged.We conclude that All stimulates the release of AVP in males and potentiates the response of AVP to the osmolar stimulus, and that oestrogen potentiates in man the release of AVP in response to the osmolar stimulus. This oestrogenic effect may account for the observed sex difference.We have previously reported that the daily urinary excretion of antidiuretic hormone was significantly elevated in male as compared with female subjects and furthermore that women presented a stronger antidiuretic hormone response to an osmotic load than did men .Little is known about the factors modulating the release of antidiuretic hormone (AVP) in human beings in response to changes in serum osmolality or in intravascular volume. Many experimental observations in animals point to a physiological link between the two systems responsible for maintain¬ ing the constancy of the body's fluid volume and composition: antidiuretic hormone regulating water balance and the renin-angiotensin-aldosterone system regulating salt balance. In dogs the infusion of angiotensin II (All) has been shown to stimulate the secretion of antidiuretic hormone and to potentiate the liberation of antidiuretic hormone in response to an osmotic load (reviewed by Share 1979). In addition to this action angioten¬ sin exerts a central dipsogenic effect as demon¬ strated by Fitzsimons 1978). Angiotensin II has been found to induce the liberation of vasopressin after intracerebroventricular injection or when In memory of the late Dr. U. Merkelbach.

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Effects of estradiol on sodium and potassium balances in adrenalectomized dogs

Cited by 21 publications

References 0 publications

Chronic Estradiol Treatment Decreases Angiotensin II Receptor Density in the Anterior Pituitary Gland and Adrenal Cortex but Not in the Mesenteric Artery

Chronic Estradiol Treatment Decreases Angiotensin II Receptor Density in the Anterior Pituitary Gland and Adrenal Cortex but Not in the Mesenteric Artery

Effects of estradiol on aldosterone secretion in ovariectomized rats

Studies of the factors modulating antidiuretic hormone excretion in man in response to the osmolar stimulus: effects of oestrogen and angiotensin II

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