Effects of Organic Antagonists of Ca2+, Na+, and K+ on Chemotaxis and Motility ofEscherichia coli

Various Ca2+ antagonists used in animal research, many of them known to be Ca2+ channel blockers, inhibitedEscherichia coli chemotaxis (measured as entry of cells into a capillary containing attractant). The most effective of these, acting in the nanomolar range, was ω-conotoxin GVIA. The next most effective were gallopamil and verapamil. At concentrations around 100-fold higher than that needed for inhibition of chemotaxis, each of these antagonists inhibited motility (measured as entry of cells into a capillary lacking attractant). Various other Ca2+antagonists were less effective, though chemotaxis was almost always more sensitive to inhibition than was motility. Cells treated with each of these Ca2+ antagonists swam with a running bias, i.e., tumbling was inhibited. Similarly, some Na+ antagonists used in animal research inhibited bacterial chemotaxis. E. coli chemotaxis was inhibited by saxitoxin at concentrations above 10−7 M, while more than 10−4 M was needed to inhibit motility. Cells treated with saxitoxin swam with a tumbling bias. In the case of other Na+ antagonists in animals, aconitine inhibited bacterial chemotaxis 10 times more effectively than it inhibited motility, and two others inhibited chemotaxis and motility at about the same concentration. In the case of K+ antagonists used in animal research, 4-aminopyridine blocked E. coli chemotaxis between 10−3 M and, totally, 10−2 M, while motility was not affected at 10−2 M; on the other hand, tetraethylammonium chloride failed to inhibit either chemotaxis or motility at 10−2 M