Mechanisms of the Enhanced Contractile Response to a Low Concentration of Phorbol 12,13-Dibutyrate in Thoracic Aorta Isolated from Rats with Dietary Magnesium Deficiency
| Autor: | Hideaki Sakaguchi, Akira Nishio, Shigeru Ishiguro, Atsushi Miyamoto, Naohiro Anai |
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| Rok vydání: | 1995 |
| Předmět: |
Male
medicine.medical_specialty Contraction (grammar) Nifedipine chemistry.chemical_element Aorta Thoracic Calcium chemistry.chemical_compound Internal medicine medicine.artery medicine Animals Thoracic aorta Magnesium Rats Wistar Enzyme inducer Phorbol 12 13-Dibutyrate Protein Kinase C Protein kinase C Pharmacology Binding Sites biology Chemistry Diet Rats Endocrinology biology.protein Phorbol Calcium Channels medicine.symptom Muscle Contraction medicine.drug Muscle contraction |
| Zdroj: | Japanese Journal of Pharmacology. 67:9-12 |
| ISSN: | 0021-5198 |
| DOI: | 10.1254/jjp.67.9 |
| Popis: | The mechanisms underlying the enhanced contractile response to phorbol 12,13-dibutyrate (PDBu) were examined in de-endothelialized thoracic aortas isolated from rats with dietary magnesium (Mg) deficiency. PDBu (1.0 nM)-induced contractions were significantly larger in Mg-deficient rats than in the controls. The contraction was completely inhibited by nifedipine, removal of external Ca2+ or by l-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7). PDBu (1.0 nM) and phorbol 12-myristate 13-acetate (1.0 μM) significantly decreased the KD value and increased the Bmax for the binding of [3H]PN200-110 to the aortas. The degree of the decrease in the KD value was significantly greater in Mg-deficient rats than in the controls. The PDBu-induced decrease in the KD value was abolished by H7. These results suggest that activation of protein kinase C by phorbol esters may participate in the activation of L-type Ca2+ channels, which increases both the affinity of [3 HJPN200-110 binding and the magnitude of the external Ca2+-dependent contraction. Dietary Mg-deficiency may enhance these processes. |
| Databáze: | OpenAIRE |
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