Abstract
IT is a well-established fact that chlorothiazide potentiates the hypotensive effects of ganglion-blocking agents1–2. However, the way this potentiation is brought about is not clear. It has been thought that chlorothiazide acts either by a direct hypotensive action2, or by sodium depletion3, or by reduction in plasma-volume3, or as in the case of mecamilamine and possibly of pempidine, by a reduction in renal excretion4 of the ganglion-blocking agents. From a pharmacological view-point there is a good deal of similarity between the neuromuscular junction and the gangliarsynapsis.
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Tapia, F. A., Dustan, H. P., et al., Lancet, ii, 831 (1957).
Hall, R., and Owen, S. G., ibid., ii, 6 (1957).
Dollery, C. T., et al., ibid., i, 1215 (1959).
Harington, M., and Kincaid-Smith, P., ibid., i, 403 (19
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FERRARI, W., GESSA, G. & SANGIORGI, G. Increase by Chlorothiazide of the Paralysing Activity of d-Tubocurarine Chloride. Nature 184, 1235 (1959). https://doi.org/10.1038/1841235a0
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DOI: https://doi.org/10.1038/1841235a0
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