Open AccessMechanisms of the Enhanced Contractile Response to a Low Concentration of Phorbol 12,13-Dibutyrate in Thoracic Aorta Isolated from Rats with Dietary Magnesium Deficiency
Author(s) -
Hideaki Sakaguchi,
Naohiro Anai,
Atsushi Miyamoto,
Shigeru Ishiguro,
Akira Nishio
Publication year - 1995
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.67.9
Subject(s) - thoracic aorta , magnesium , aorta , medicine , endocrinology , magnesium deficiency (plants) , chemistry , biology , anatomy , organic chemistry
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 microM) 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 Ca(2+)-dependent contraction. Dietary Mg-deficiency may enhance these processes.