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

[摘要] References(29)Cited-By(1)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 (1.0μM) 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 [3H]PN200-110 binding and the magnitude of the external Ca2+-dependent contraction. Dietary Mg-deficiency may enhance these processes.

[学科分类] 药理学

[关键词] Mg-deficient rat;Phorbol 12;13-dibutyrate;Protein kinase C;[3H]PN200-110 binding;Ca2- channel