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Bloat from roids.


oswaldosalcedo
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Androgens augments vasopressin (AVP) release.

Non osmotic AVP release in adrenal insuffiency by glucorticoid antagonism produced by supraphysiological androgen.

Oswaldo Salcedo.

A posible mechanism responsible for water retention is induced Hypopituitarism (reduced output of any pituitary hormone) by displaced Glucocorticoids (GC) through Androgens at the GC receptors at Pituitary, acting by antagonist mode, therefore decreasing Corticotropin (ACTH). Subsequent to the ACTH decreased secretion, inhibits cortisol segregation at adrenals (Central Hypoadrenalism - Secondary Adrenal Insufficiency). The cortisol suppression produces in the hypothalamus, vasopressin (AVP) release, also known like anti diuretic hormone (ADH), this way GC insufficiency increases AVP mRNA expression, elevating abnormally AVP levels,free water retention, decreased sodium pump activity, shift of extracellular sodium into cells and decreased delivery of filtrate to diluting segments of the nephron as a result of decreased glomerular filtration rate and effective renal plasma flow.GC inhibit AVP secretion by impairing AVP gene transcription.

J Neuroendocrinol. 2001 May;13(5):442-52.

Androgens alter corticotropin releasing hormone and arginine vasopressin mRNA within forebrain sites known to regulate activity in the hypothalamic-pituitary-adrenal axis.

Viau V, Soriano L, Dallman MF.

Department of Physiology, University of California, San Francisco 94143-0444, USA.

To reveal direct effects of androgens, independent of glucocorticoids, we studied the effects of gonadectomy (GDX) in adrenalectomized (ADX) rats with or without androgen replacement on corticotropin releasing hormone (CRH) and arginine vasopressin (AVP) mRNA expression within various forebrain sites known to regulate the hypothalamic-pituitary-adrenal axis. These included the medial parvocellular portion of the paraventricular nucleus of the hypothalamus (mp PVN), the central and medial nuclei of the amygdala and bed nuclei of the stria terminalis (BNST). In the mp PVN, ADX stimulated both CRH and AVP mRNA expression. Combined ADX + GDX inhibited only AVP, and Testosterone and dihydrotestosterone (DHT) restored AVP mRNA. In the central nucleus of the amygdala, ADX decreased CRH mRNA expression, and this response was unaffected by GDX +/- testosterone or DHT replacement. In the medial amygdala, AVP mRNA expression was decreased by ADX, abolished by ADX + GDX, and restored by androgen replacement. ADX had no effect on CRH and AVP mRNA expression in the BNST. GDX + ADX, however, reduced CRH mRNA expression only within the fusiform nuclei of the BNST and reduced the number of AVP-expressing neurones in the posterior BNST. Androgen replacement reversed both responses. In summary, in ADX rats, AVP, but not CRH mRNA expression in the amygdala and mp PVN, is sensitive to GDX +/- androgen replacement. Both CRH- and AVP-expressing neurones in the BNST respond to GDX and androgen replacement, but not to ADX alone. Because androgen receptors are not expressed by hypophysiotropic PVN neurones, we conclude that glucocorticoid-independent, androgenic influences on medial parvocellular AVP mRNA expression are mediated upstream from the PVN, and may involve AVP-related pathways in the medial amygdala, relayed to and through CRH- and AVP-expressing neurones of the BNST.

Am J Kidney Dis. 2006 May;47(5):727-37.

Vasopressin excess and hyponatremia.

Pham PC.

Nephrology Division, Olive View-UCLA Medical Center, Sylmar, CA 91342, USA.

Hyponatremia is a common electrolyte disorder that frequently is overlooked and undertreated. Although the pathophysiological process of hyponatremia is complex, arginine vasopressin (AVP) is a common etiologic factor. Excess AVP release by osmotic or nonosmotic stimuli or both can lead to sodium and water imbalance. Conventional treatment options for hyponatremia, including water restriction and administration of sodium chloride with or without loop diuretics, do not directly address the underlying water retention induced by excess AVP in many cases. Clinical trials showed that AVP-receptor antagonists, including lixivaptan, tolvaptan, and conivaptan, produce aquaresis, the electrolyte-sparing excretion of free water, to correct serum sodium concentration. We review results from recent clinical trials involving AVP-receptor antagonists in the treatment of hyponatremia associated with AVP excess.

of course, i have postulated other mechanisms,valid in other conditions,estradiol,progesterone,thiroxine,gh, etc, each one are unique with his conditions and particular mechanics.

dr frankenstein


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Tazmaniac
(@tazmaniac)
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Get you some aromasin

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Information that Tazmaniac presents is totally fictitious in nature and is presented for role playing purposes only. The opinions presented do not encourage the use of illegal substances nor take the place of professional medical advice.

Death gotta be easy, cause life is hard...it'll leave you physically, mentally, and emotionally scarred~50 Cent


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oswaldosalcedo
(@oswaldosalcedo)
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Topic starter  
Posted by: Tazmaniac
Get you some Aromasin

thanks, but i have very low levels of estradiol,around 8 pg/ml and 14 pg/ml (normal levels 10 pg/ml-50 pg/ml).

dr frankenstein


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oswaldosalcedo
(@oswaldosalcedo)
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J Neurosci. 1994 Mar;14(3 Pt 2):1789-94.

Sex differences in the effects of testosterone and its metabolites on vasopressin messenger RNA levels in the bed nucleus of the stria terminalis of rats.

De Vries GJ, Wang Z, Bullock NA, Numan S.

Department of Psychology, University of Massachusetts, Amherst 01003.

Male rats have about two times as many steroid-responsive vasopressin-immunoreactive (AVP-ir) neurons in the bed nucleus of the stria terminalis (BST) as female rats. This sex difference does not depend on differences in circulating hormone levels, since it persists in males and females that are treated with similar levels of testosterone. To analyze the cellular basis of this sex difference, we compared the effects of testosterone and its metabolites on AVP mRNA expression in the BST of males and females that were gonadectomized at 3 months of age. When rats received implants of Silastic tubing filled with testosterone, males had more cells that were labeled for AVP mRNA and more labeling per cell than females

dr frankenstein


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oswaldosalcedo
(@oswaldosalcedo)
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Reprod Domest Anim. 2006 Dec;41(6):514-21.

Oestradiol Stimulates the Release of AVP and GnRH from the Ewe Hypothalamus In Vitro.

Ghuman S, Prabhakar S, Smith R, Dobson H.

Department of Veterinary Clinical Science, University of Liverpool, Leahurst, Neston, Wirral, UK.

Oestradiol (E(2)) sensitizes the stress and reproductive axes in vivo. Our current aim is to investigate whether E(2) directly influences hypothalamic AVP and GnRH release in vitro. Within 10 min of ewe killing, saggital midline hypothalamic slices (from the anterior preoptic area to mediobasal hypothalamus, 2 mm thick, two per sheep) were dissected, placed in oxygenated MEM-alpha at 4 degrees C and within next 2 h were singly perifused at 37 degrees C with oxygenated MEM-alpha (pH 7.4; flow rate 150 mul/min) alone (vehicle; n = 15), with low (6 pg/ml; n = 14) or high E(2) (24 pg/ml; n = 13). After 5 h equilibration, 10 min fractions were collected for 3 h with exposure to 100 mm KCl for 10 min within the last hour. Concentrations of AVP and GnRH were measured by RIA. Baselines for AVP and GnRH were 7.0 +/- 1.1 and 17.4 +/- 0.8 pg/ml respectively. Basal values with low E(2) were similar to vehicle for AVP (7.5 +/- 1.2 pg/ml) and GnRH (17.5 +/- 1.1 pg/ml). However, high E(2) increased basal AVP (11.7 +/- 1.4 pg/ml; p < 0.05) and GnRH (23.7 +/- 1.4 pg/ml; p < 0.05). After KCl, AVP and GnRH respectively, increased (p < 0.05) to 25.6 +/- 7.5 and 38.2 +/- 5.6 (vehicle), 26.3 +/- 7.5 and 23.6 +/- 2.1 (low E(2)) and 24.1 +/- 5.4 and 41.3 +/- 6.6 pg/ml (high E(2)). After KCl, maximum values of AVP occurred at 20 and GnRH at 30 min. In conclusion, high E(2) concentration augments AVP and GnRH release by direct action on the ewe hypothalamus.

Am J Physiol Endocrinol Metab. 2002 Oct;283(4):E711-21.

Estrogen effects on osmotic regulation of AVP and fluid balance.

Stachenfeld NS, Keefe DL.

The John B. Pierce Laboratory and Departments of Epidemiology and Public Health, Yale University School of Medicine and Women and Infants Hospital, Brown University School of Medicine, New Haven, Connecticut 06519, USA.

To determine estrogen effects on osmotic regulation of arginine vasopressin (AVP) and body fluids, we suppressed endogenous estrogen and progesterone using the gonadotropin-releasing hormone (GnRH) analog leuprolide acetate (GnRHa). Subjects were assigned to one of two groups: 1) GnRHa alone, then GnRHa + estrogen (E, n = 9, 25 +/- 1 yr); 2) GnRHa alone, then GnRHa + estrogen with progesterone (E/P, n = 6, 26 +/- 3). During GnRHa alone and with hormone treatment, we compared AVP and body fluid regulatory responses to 3% NaCl infusion (HSI, 120 min, 0.1 ml. min(-1). kg body wt(-1)), drinking (30 min, 15 ml/kg body wt), and recovery (60 min of seated rest). Plasma [E(2)] increased from 23.9 to 275.3 pg/ml with hormone treatments. Plasma [P(4)] increased from 0.6 to 5.7 ng/ml during E/P and was unchanged (0.4 to 0.6 ng/ml) during E. Compared with GnRHa alone, E reduced osmotic AVP release threshold (275 +/- 4 to 271 +/- 4 mosmol/kg, P < 0.05), and E/P reduced the AVP increase in response during HSI (6.0 +/- 1.3 to 4.2 +/- 0.6 pg/ml at the end of HSI), but free water clearance was unaffected in either group. Relative to GnRHa, pre-HSI plasma renin activity (PRA) was greater during E (0.8 +/- 0.1 vs. 1.2 +/- 0.2 ng ANG I. ml(-1). h(-1)) but not after HSI or recovery. PRA was greater than GnRHa during E/P at baseline (1.1 +/- 0.2 vs. 2.5 +/- 0.6) and after HSI (0.6 +/- 0.1 vs. 1.1 +/- 1.1) and recovery (0.5 +/- 0.1 vs. 1.3 +/- 0.2 ng ANG I. ml(-1). h(-1)). Baseline fractional excretion of sodium was unaffected by E or E/P but was attenuated by the end of recovery for both E (3.3 +/- 0.6 vs. 2.4 +/- 0.4%) and E/P (2.8 +/- 0.4 vs 1.7 +/- 0.4%, GnRHa alone and with hormone treatment, respectively). Fluid retention increased with both hormone treatments. Renal sensitivity to AVP may be lower during E due to intrarenal effects on water and sodium excretion.

J Appl Physiol. 2001 Oct;91(4):1893-901.

Sex differences in osmotic regulation of AVP and renal sodium handling.

Stachenfeld NS, Splenser AE, Calzone WL, Taylor MP, Keefe DL.

The John B. Pierce Laboratory, Yale University School of Medicine, 290 Congress Ave., New Haven, Connecticut 06519, USA.

To determine sex differences in osmoregulation of arginine vasopressin (AVP) and body water, we studied eight men (24 +/- 1 yr) and eight women (29 +/- 2 yr) during 3% NaCl infusion [hypertonic saline infusion (HSI); 120 min, 0.1 ml. kg body wt(-1). min(-1)]. Subjects then drank 15 ml/kg body wt over 30 min followed by 60 min of rest. Women were studied in the early follicular (F; 16.1 +/- 2.8 pg/ml plasma 17beta-estradiol and 0.6 +/- 0.1 ng/ml plasma progesterone) and midluteal (L; 80.6 +/- 11.4 pg/ml plasma 17beta-estradiol and 12.7 +/- 0.7 ng/ml plasma progesterone) menstrual phases. Basal plasma osmolality was higher in F (286 +/- 1 mosmol/kgH(2)O) and in men (289 +/- 1 mosmol/kgH(2)O) compared with L (280 +/- 1 mosmol/kgH(2)O, P < 0.05). Neither menstrual phase nor gender affected basal plasma AVP concentration (P([AVP]); 1.7 +/- 4, 1.9 +/- 0.4, and 2.2 +/- 0.5 pg/ml for F, L, and men, respectively). The plasma osmolality threshold for AVP release was lowest in L (x-intercept, 263 +/- 3 mosmol/kgH(2)O, P < 0.05) compared with F (273 +/- 2 mosmol/kgH(2)O) and men (270 +/- 4 mosmol/kgH(2)O) during HSI. Men had greater P([AVP])-plasma osmolality slopes (i.e., sensitivity) compared with F and L (slopes = 0.14 +/- 0.04, 0.09 +/- 0.01, and 0.24 +/- 0.07 for F, L, and men, respectively, P < 0.05). Despite similar Na+-regulating hormone responses, men excreted less Na+ during HSI (0.7 +/- 0.1, 0.7 +/- 0.1, and 0.5 +/- 0.1 meq/kg body wt for F, L, and men, respectively, P < 0.05). Furthermore, men had greater systolic blood pressure (119 +/- 5, 119 +/- 5, and 132 +/- 3 mmHg for F, L, and men, respectively, P < 0.05) than F and L. Our data indicate greater sensitivity in P([AVP]) response to changes in plasma osmolality as the primary difference between men and women during HSI. In men, this greater sensitivity was associated with an increase in systolic blood pressure and pulse pressure during HSI, most likely due to a shift in the pressure-natriuresis curve.

dr frankenstein


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