GNRH ANALOGLAR PDF

Since then, numerous studies have shown that a permanent lowering of the testosterone level, e. This has been proven in recent studies. In addition, hormone withdrawal with GNRH analogues continues to provide the basic therapy for new treatment options, e. Seither zeigen zahlreiche Untersuchungen, dass mit einer dauerhaften Senkung des Testosteronspiegels, wie z. Apalutamid dar. This site needs JavaScript to work properly.

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The physiological actions and clinical applications of gonadotropin-releasing hormon GnRH and its analogues have received increasing attention within the past few years. The hypothalamic decapeptide GnRH stimulates the syntheseis and secretion of luteinizing hormon LH and follicle-stimulating hormon FSH , responsible for the cyclic changes and ovarian steroid production of the female menstrual cycle. The intracellular pathway through which GnRH stimulates pituitary gonadotroph function is receptor-mediated and calcium dependent.

Recently we and others have focused our attention on the transmembrane signaling involved in GnRH action. The native hormone GnRH binds to specific receptors on the surface of the pituitary cell membrane. This receptor is coupled to the formation of second messengers participating in hormonal exocytosis.

The activation of the GnRH receptor will cause the hydrolysis of phos-phoinositides within 5 seconds. The breakdown of these membrane lipids will produce inositolphosphates and diacylglycerol. We have identified specific membrane-bound receptors for inositol-1,4,5-triphosphate in pituitary cells. Inositolphosphates can rapidly release calcium from intracellular stores or promote calcium influx. The release of gonadotropins and the function of pituitary gonadotrophs is highly calcium-dependent.

In vitro experiments have demonstrated that GnRH stimulation will activate the liberation of arachidonic acid from lipid stores and this fatty acid is readily metabolized to lipoxygenase products such as leuko-trienes in the pituitary cell. Leukotrienes are potent mediators and modulators of GnRH action.

A further pathway in the cascade of signal transduction appears to be relevant in the pituitary. This involves the translocation and activation of the calcium- and phospholipid-dependent proteinkinase C. The activation of this enzyme by phorbolesters can induce a prolongued gonadotropin secretion in vitro. At present, however, it quite unclear how the different cascades orchestrate hormonal exocytosis. GnRH-analogues have a paradoxical effect on gonadotroph function.

The long-term action of potent GnRH analogues will result in the down-regulation of. GnRH-receptors and will cause desensitisation of the pituitary. In vitro experiments suggest that down-regulation of GnRH-receptors may represent only one aspect of the phenomenon of desensitisation due to prolongued action of GnRH in vivo and in vitro.

Several other intracellular sites of action have been proposed including the uncoupling of the GnRH-receptor from the guanine nucleotide regulatory protein and from phospholipase C. Desensitisation evoked by GnRH-agonist is preceded by a short phase of receptor up-regulation and pituitary stimulation. GnRH antagonists will act on the pituitary by competitive binding to the GnRH-receptor without inducing the synthesis or secretion of gonadotropins. The application of GnRH-anlogues produces thereby a reversible inhibition of gonadotroph function and ovarian suppression.

Their use has opened a wide field of medical treatment of hormone dependent the benign and malignant diseases in gynecology. Unable to display preview. Download preview PDF. Skip to main content. This service is more advanced with JavaScript available. Advertisement Hide. Authors Authors and affiliations L. Kiesel B. Conference paper. Abstract The physiological actions and clinical applications of gonadotropin-releasing hormon GnRH and its analogues have received increasing attention within the past few years.

The long-term action of potent GnRH analogues will result in the down-regulation of GnRH-receptors and will cause desensitisation of the pituitary. This is a preview of subscription content, log in to check access. Clayton RN, Catt KJ Gonadotropin-releasing hormone receptors: characterization, physiological regulation and relationship to reproductive function. Huckle WR, Conn PM The relationship between gonadotropin-releasing hormone-stimulated luteinizing hormone release and inositol phosphate production: studies with calcium antagonists and proteinkinase C activators.

Kiesel L, Bertges K, Rabe T, Runnebaum Gonadotropin-releasing hormone enhances polyphosphoinositide hydrolysis in rat pituitary cells.

Kiesel, L. Endocrinology — Google Scholar. Naor Z, Kiesel L, Vanderhoek J, Catt KJ Mechanism of action of gonadtropin-releasing hormone: role of lipoxygenase products of arachidonic acid in luteinizing hormone release. Nishizuka Y The role of proteinkinase C in cell surface signal transduction and tumor promotion. Smith, Vale Desensitization of gonadotropin-releasing hormone observed in superfused pituitary cells on cytodex beads.

Wildt L Die endokrine Kontrolle des menstruellen Zyklus. Enke, Stuttgart, S 1—25 Google Scholar. Kiesel 1 B. Runnebaum 1 1. Personalised recommendations. Cite paper How to cite? ENW EndNote.

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Entwicklung und Anwendung der GnRH-Analoga in der Sterilitätstherapie

Dies scheint der wesentliche Vorteil der GnRH-Antagonisten zu sein, die sich zur Zeit noch in klinisch experimenteller Erprobung befinden. GnRH plays a pivotal role in the control of the Ovarian cycle. The hormone consists of ten aminoacids decapeptide. By modifying the molecular structure Compounds with either stimulatory agonists or inhibitory antagonists effects were optained. This is caused by a reduction in the number of GnRH receptors on the cell membrane and uncoupling of the receptor from Signal transduction into the cell. The pituitary becomes refractory to hypothalamic GnRH.

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Steuerung der Hypophysenfunktion durch das Gonadotropin-Releasing Hormon (GnRH) und dessen Analoga

The physiological actions and clinical applications of gonadotropin-releasing hormon GnRH and its analogues have received increasing attention within the past few years. The hypothalamic decapeptide GnRH stimulates the syntheseis and secretion of luteinizing hormon LH and follicle-stimulating hormon FSH , responsible for the cyclic changes and ovarian steroid production of the female menstrual cycle. The intracellular pathway through which GnRH stimulates pituitary gonadotroph function is receptor-mediated and calcium dependent. Recently we and others have focused our attention on the transmembrane signaling involved in GnRH action.

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