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

Abstract

ABSTRACT-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 Ca 21 or by 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7). PDBu (1.0 nM) and phorbol 12-myristate 13-acetate (1.0 pM) 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 Ca 21 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.

Bovine lactoferrin has a nitric oxide-dependent hypotensive effect in rats

“…Each ring was mounted in an organ bath containing 5 ml physiological solution (PSS) with the following composition (in mM): 119 NaCl, 4.7 KCl, 2.5 CaCl 2, 1.2 MgCl2, 1.2 KH2PO4, 25 NaHCO3, and 10 glucose. The organ bath solution was maintained at 37°C and gassed with 95% O 2-5% CO2 (35). Each ring was left to equilibrate for at least 2 h under a resting tension of 10 mN, which was kept constant throughout the experiment.…”