Increased Rho-kinase-mediated prostate contractions associated with impairment of β-adrenergic-cAMP-signaling pathway by chronic nitric oxide deficiency
| Autor: | Fabíola Z. Mónica, Edson Antunes, Marcos José Alves Junior, Luiz O. Leiria, Fernando R. Báu, Fábio H. Silva, Fabiano B. Calmasini, Eduardo C. Alexandre |
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| Jazyk: | angličtina |
| Předmět: |
Male
Nitroprusside Agonist Beta-adrenergic pathway medicine.medical_specialty Carbachol Pyridines medicine.drug_class Stimulation Muscarinic agonist Nitric oxide Phenylephrine chemistry.chemical_compound Adenosine Triphosphate L-NAME Internal medicine Cyclic AMP medicine Animals Rho-kinase Receptor Cyclic GMP Pharmacology rho-Associated Kinases Dose-Response Relationship Drug Isoproterenol Prostate Muscle Smooth Amides Electric Stimulation Rats NG-Nitroarginine Methyl Ester Endocrinology chemistry Sodium nitroprusside Muscle Contraction Signal Transduction medicine.drug |
| Zdroj: | European Journal of Pharmacology. :24-30 |
| ISSN: | 0014-2999 |
| DOI: | 10.1016/j.ejphar.2015.03.057 |
| Popis: | Impairment of nitric oxide (NO) – cyclic GMP signaling pathway is likely to contribute to human begnin prostate hyperplasia (BPH). In the present study we have used a model of chronic NO synthesis inhibition to evaluate the functional alterations of prostate smooth muscle (PSM) machinery, and involvement of Rho-kinase pathway. Wistar rats were treated with the NO inhibitor Nω-nitro-l-arginine methyl ester (L-NAME, 20 mg/kg/day; 4 weeks), after which contractile responses to phenylephrine (α1-adrenoceptor agonist; 1 nM to 100 µM), carbachol (muscarinic agonist; 1 nM to 1 mM) and α,β-methylene ATP (P2X receptor agonist; 1–10 µM), as well as to electrical-field stimulation (EFS; 1–32 Hz) were evaluated. PSM relaxations to isoproterenol (non-selective β-adrenoceptor agonist, 0.1 nM to 10 µM) and sodium nitroprusside (NO donor, 1 nM to 10 mM) were also evaluated. The ratio prostate weight/body weight was 22% greater (P |
| Databáze: | OpenAIRE |
| Externí odkaz: |
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