CHRONIC PROPRANOLOL TREATMENT CAUSES DESENSITIZATION OF THE STEROIDOGENIC RESPONSE IN TESTICULAR INTERSTITIAL CELLS BUT DOES NOT ALTER PROTEIN KINASE C
| Autor: | Maria I. Wanderley, Juliany S. B. César Vieira, Daniel P. Udrisar, D. M. C. Rego, Maria do Carmo de Carvalho e Martins |
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| Rok vydání: | 2006 |
| Předmět: |
Male
endocrine system medicine.medical_specialty Down-Regulation Enzyme Activators Propranolol Biology Testicle Interstitial cell chemistry.chemical_compound Endocrinology Internal medicine medicine Animals Testosterone Secretion Rats Wistar Protein kinase A Antihypertensive Agents Protein Kinase C Protein kinase C Dose-Response Relationship Drug Leydig cell Leydig Cells Cyclic AMP-Dependent Protein Kinases Rats medicine.anatomical_structure chemistry Phorbol medicine.drug |
| Zdroj: | Archives of Andrology. 52:215-221 |
| ISSN: | 0148-5016 |
| DOI: | 10.1080/01485010500397931 |
| Popis: | We investigated effects of chronic propranolol treatment on the secretory response of rat testicular interstitial cells (testosterone secretion) to subsequent in vitro stimulation with activators of protein kinase-C (PK-C) (L-propranolol, phorbol 12, 13-dibutyrate (PDBu), LHRH) or activators of protein kinase A (PK-A), (hCG or dibutyryl cAMP (dbcAMP)). We determined [3H]PDBu binding and PK-C activity in these cells. Treatment of rats with propranolol (Inderal 500 mg/L of water for 5 weeks) reduced by 48%, 50% and 29% the L-propranolol-, LHRH- or PDBu-induced testosterone secretion, respectively, when compared to cells from controls. This desensitization in testosterone secretion in vitro was also present when the testicular interstitial cells were stimulated with hCG or dbcAMP (secretion decreased by 65%/57%, respectively, when compared to cells from control rats). Challenging the cells originated from rats that received propranolol chronically with the addition in vitro of propranolol resulted in an additional reduction of the hCG/dbcAMP-stimulated testosterone secretion. Chronic propranolol-induced desensitization was not associated with a loss in [3H]PDBu binding or a decrease in PK-C activity. Chronic propranolol-induced desensitization can be uncoupled from down-regulation of protein kinase C. The effector responsible for the desensitization could be distal to the protein kinase C and protein kinase A. |
| Databáze: | OpenAIRE |
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