International Journal of Biomedicine (Jun 2019)
Blocking L-type Voltage-Gated Calcium Ion Channels Changes the Intensity of Protein Synthesis in Metanephric Cells
Abstract
The purpose of this research was to study the effect of L-type voltage-gated calcium channels (L-VGCC) blocking on mRNA content and intensity of protein synthesis in cells of the metanephros. Materials and Methods: The study was performed on 27 outbred Wistar rats weighing 250-270 g from 5 to 7 months of age. Pregnant females were divided into 3 groups of 9 individuals each. Group1 (the control group) included intact pregnant females treated with distilled water; Group 2 (the first experimental group) included animals receiving a therapeutic dose of nifedipine; Group 3 (the second experimental group) included animals receiving a toxic dose of nifedipine. The dihydropyridine nifedipine (Sigma-Aldrich, Gillingham, UK) was used as a Ca2+ channel blocker. Nifedipine was dissolved in distilled water. The dose of nifedipine was calculated based on therapeutic and toxic doses for humans. The therapeutic dose for rats was 127 mg/kg, toxic dose – 762 mg/kg. In each group, when rats reached Day 14, 15, 16 and consistently up to 22 of gestation, they were removed from the experiment by decapitation under ether anesthesia. The embryos and fetuses were removed, subjected to external examination and quickly fixed with 10% neutral formalin entirely up to the age of 15 days. At an older age, both metanephros were removed from the fetuses by preparation and fixed with 10% neutral formalin. The intensity of protein synthesis was estimated by the content of mRNA in the cytoplasm. Results: The development of the metanephros in rats of the control group was accompanied by a gradual decrease in the content of mRNA, indicating the activity of protein synthesis in the cell cytoplasm of epithelial and mesenchymal buds of the metanephros. In the fetuses of rats whose mothers received therapeutic and toxic doses of nifedipine, statistically significant changes in the content of mRNA in the cytoplasm of the metanephric cells were observed. These changes were most significant in the metanephric cells after administration of the toxic dose. On ED 17, an L-VGCC blockade with a therapeutic dose of nifedipine led to a paradoxical reaction of cells with an increase in protein synthesis, compared with the control group. Conclusion: Both doses of nifedipine have a greater effect on the content of mRNA in the cytoplasm of epithelial cells, compared to mesenchymal buds.
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