Aqui agrego otra informacion posteada por pincho42 en ese thread,valiosa.
La aminogluthemida (orimeten,cytadren etc) inhibe el primer paso en la generacion de las hormonas al inhibir la accion de la enzima CPY11A1 (desmolasa) sobre el colesterol en la conversion a pregnenolona al inhibir este primer paso se inhibe de una vez la subsecuente conversion y produccion de todas las hormonas de base steroidales ,no peptidas como insulina,human growth hormone - somatropin - y otras.
Es decir se inhibe la dehidroepiandrosterona,progesterona,androstenodiona,cortiscosterona,cortisol,aldosterona,testosterona etc.
uno queda en un estado de disminucion esteroidal,pero no importa porque puedes suministrar testosterona (el ciclo pues) y si baja demasiado el cortisol debes administrar algo de cortisol para que no se cree un insuficiencia adrenal y asi con las demas. Ahora, uno no podria usar esta droga en una etapa PCT - post cycle therapy - - post cycle therapy - - post cycle therapy - pero si durante un ciclo,se comenta que andreas munzer la usaba frecuentemente (para mi uno de los bodybuilders mas estriados y rallados que jamas se haya visto) pero que tambien tuvo que pagar un precio muy alto,igual la siguen usando muchos,pero hay otras opciones por supuesto,recuerda que el fisicoculturismo es evoluciony evolucion
voy a hacer una descripcion succcinta sobre ellas
Adreocorticolicos:
Mitotane:
Un derivado del insecticida DDT, el DDD el cual produce necrosis en la zona fascicular y la reticular,zonas productoras de esteroides adrenales.
Inhibicion Enzimatica
.-Inhibicion de la CPY11A1: Aminoglutemida.
.-Inhibicion de la CYP11B1: Metyrapone, esta enzima cyp11b1 cataliza el ultimo paso en la conversion del 11-Deoxycortisol a cortisol tambien inhibe la secrecion de aldosterona la inhibir la enzima CPY11B2.
.-Inhibicion de la 3Beta-HSD: Cyanocetona
.-Inhibicion Multiple: Ketoconazole y Etomidato esta son drogas antifungales que actuan sobre el sistema p450
inhibiendo en varias etapas a las enzimas,por lo general CPY11B1 y CPY11A1 entre otras.
Bloqueo de la accion del cortisol:
Mifrepristone.
Lilopristone.
Onanipristone.
estos antagonistas del cortisol se ligan a los receptores y evitan asi la accion posterior de estos receptores.
Por lo momentos lo dejamos asi si hay algun punto en particular sirvete preguntar con toda libertad.
no posteo los estuidos porque duro otra hora mas, ja !
Volviendo al punto de los bloqeuadores de la angiotensina:
con mas detale para el amigo J.C y a todos los que les gusta profundizar.
J Biol Chem. 1995 Sep 8;270(36):20942-51.
Losartan-sensitive AII receptors linked to depolarization-dependent cortisol secretion through a novel signaling pathway.
Mlinar B, Biagi BA, Enyeart JJ.
Department of Pharmacology, Ohio State University, College of Medicine, Columbus 43210-1239, USA.
In bovine adrenal zona fasciculata (AZF) cells, angiotensin II (AII) may stimulate depolarization-dependent Ca2+ entry and cortisol secretion through inhibition of a novel potassium channel (IAC),which appears to set the resting potential of these cells. Aspects of the signaling pathway, which couples AII receptors to membrane depolarization and secretion, were characterized in patch clamp and membrane potential recordings and in secretion studies. AII-mediated inhibition of IAC, membrane depolarization, and cortisol secretion were all blocked by the AII type I (AT1) receptor antagonist losartan. These responses were unaffected by the AT2 antagonist PD123319. Inhibition of IAC by AII was prevented by intracellular application of guanosine 5'-O-2-(thio)-diphosphate but was not affected by pre-incubation of cells with pertussis toxin. Although mediated through an AT1 receptor, several lines of evidence indicated that AII inhibition of IAC occurred through an unusual phospholipase C (PLC)-independent pathway. Acetylcholine, which activates PLC in AZF cells, did not inhibit IAC. Neither the PLC antagonist neomycin nor PLC-generated second messengers prevented IAC expression or mimicked the inhibition of this current by AII. IAC expression and inhibition by AII were insensitive to variations in intracellular or extracellular Ca2+ concentration. AII-mediated inhibition of IAC was markedly reduced by the non-hydrolyzable ATP analog adenosine 5'-(beta, gamma-imino)triphosphate and by the non-selective protein kinase inhibitor staurosporine. The protein phosphatase antagonist okadaic acid reversibly inhibited IAC in whole cell recordings. These findings indicate that AII-stimulated effects on IAC current, membrane voltage, and cortisol secretion are linked through a common AT1 receptor.Inhibition of IAC in AZF cells appears to occur through a novel signaling pathway, which may include a losartan-sensitive AT1 receptor coupled through a pertussis-insensitive G protein to a staurosporine-sensitive protein kinase. Apparently, the mechanism linking AT1 receptors to IAC inhibition and Ca2+ influx in adrenocortical cells is separate from that involving inositol trisphosphate-stimulated Ca2+ release from intracellular stores. AII-stimulated cortisol secretion may occur through distinct parallel signaling pathways.
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Concatenando consistencia y logica
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Neuropsychopharmacology. 2005 Oct;30(10):1906-12.
Testosterone suppression of CRH-stimulated cortisol in men.
Rubinow DR, Roca CA, Schmidt PJ, Danaceau MA, Putnam K, Cizza G, Chrousos G, Nieman L.
Behavioral Endocrinology Branch, National Institute of Mental Health, Building 10-CRC, 10 Center Drive MSC 1276, Bethesda, MD 20892-1276, USA.
Despite observations of age-dependent sexual dimorphisms in hypothalamic-pituitary-adrenal (HPA) axis activity, the role of androgens in the regulation of HPA axis activity in men has not been examined. We assessed this role by performing CRH stimulation tests in 10 men (ages 18-45 years) during gonadal suppression with leuprolide acetate and during testosterone addition to leuprolide. CRH-stimulated cortisol levels as well as peak cortisol and greatest cortisol excursion were significantly lower (p<0.05, 0.005, and 0.01, respectively) during testosterone replacement compared with the induced hypogonadal condition (leuprolide plus placebo); cortisol area under the curve was lower at a trend level (p<0.1). Paradoxically, CRH-stimulated corticotropin (ACTH) was increased significantly during testosterone replacement (p<0.05). The cortisol : ACTH ratio, a measure of adrenal sensitivity, was lower during testosterone replacement (p<0.1). A mixed effects regression model showed that testosterone but not estradiol or CBG significantly contributed to the variance of cortisol. These data demonstrate that testosterone regulates CRH-stimulated HPA axis activity in men, with the divergent effects on ACTH and cortisol suggesting a peripheral (adrenal) locus for the suppressive effects on cortisol. Our results further demonstrate that the enhanced stimulated HPA axis activity previously described in young men compared with young women cannot be ascribed to an activational upregulation of the axis by testosterone.
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Porque?
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Am J Physiol Renal Physiol. 2004 Sep;287(3):F452-9.
Androgens augment proximal tubule transport.
Quan A, Chakravarty S, Chen JK, Chen JC, Loleh S, Saini N, Harris RC, Capdevila J, Quigley R.
Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9063, USA.
................the increased proximal tubule volume reabsorption would increase extracellular volume and suppress systemic angiotensin II levels. A rise in extracellular volume in the dihydrotestosterone-treated animals would be consistent with three of our findings, including hypertension, increased weight gain, and lower serum angiotensin II levels. Weight gain over the 10-day period of dihydrotestosterone/vehicle injections was twofold higher in the androgen-treated animals (75 ± 13 vs. 37 ± 12 g, P < 0.05), and MAP in androgen-treated animals was 18% higher, as shown in Fig. 1 (104 ± 2 vs. 88 ± 4 mmHg, P < 0.005). Androgens may augment proximal tubule volume reabsorption via the proximal tubule renin-angiotensin system and raise extracellular volume and blood pressure.
..............lowers serum angiotensin II levels. The dihydrotestosterone-associated increase in proximal tubule transport results from upregulation of the effect of intraluminal angiotensin II and subsequent upregulation of NHE3. These results suggest that androgens can augment proximal transport by stimulation of the proximal tubule renin-angiotensin system and may contribute to higher blood pressure.
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Asi pues vemos que explicar algo lleva tiempo,imaginense cuanto lleva aprenderlo y entenderlo!
por eso estoy totalmente encontra de lo que yo llamo "PARROTS" es decir que repiten como loritos sin haber leido lo que se dice nada! y porque? pues porque no tienen los libros o no investigan en los journals y diversas fuentes,es decir que hay que estudiar e investigar antes de hablar!
Yo tomo 80 mg de telmisartan (micardis) diarios,un antagonista de la angiotensina mas avanzado que el losartan,
me ayuda mucho aparte de lo del cortisol (en PCT) a disminuir la retencion de liquido facial (En ciclo).
Facial, Porque?
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Cardiovasc Res. 2006 Dec 1;72(3):456-63.
Androgens potentiate renal vascular responses to angiotensin II via amplification of the Rho kinase signaling pathway.
OBJECTIVES: This study assessed whether the Rho kinase signaling pathway contributes to androgenic amplification of angiotensin II (Ang II) induced pressor and renal constrictor responses.
Song J, Kost CK Jr, Martin DS.
J Hypertens. 2007 Feb;25(2):399-406.
Pressor response induced by central angiotensin II is mediated by activation of Rho/Rho-kinase pathway via AT1 receptors.
Sagara Y, Hirooka Y, Nozoe M, Ito K, Kimura Y, Sunagawa K.
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Y donde haya receptores de la angiotensina y lo que quede de angiotensina asi sea poca.
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Respecto a las opciones no clasicas a que te refieres con no clasico?,digo para no redundar pues.
Ya se ve de manera clara que los antagonistas de la angotensina son muy seguros y efectivos y se pueden usar tanto en ciclo como en PCT.
Pero por supuesto hay otros mas como los flavonoides.
Sirvete preguntar con libertad sobre lo que sea,antiestrogenicos,insulina,pgf2a,human growth hormone - somatropin - ,igf,prolactina etc
Informacion sobre "ciclitos" no me motiva mucho que se diga, pero igual va pues!
Saludos.
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