ABSTRACT
Yet new functions are still being uncovered, and this is prompting the development of new drugs that target histamine.
Histamine results from the decarboxylation of histidine, and was first described synthetically by Windaus and Vogt in 1907 (Windaus and Vogt 1907). Shortly thereafter, Dale and colleagues found that it was a natural constituent of ergot, which was potent in inducing contraction of certain muscles (Barger and Dale 1910; Dale and Laidlaw 1911). Further work suggested that the effects of histamine were similar to those seen with anaphylaxis (Dale and Laidlaw 1911). Interestingly, Dale did not use the obvious name, histamine, as he explained in his memoirs (Dale 1953), because it was claimed to be too similar to a trademark; Dale instead used the chemical name β-iminazolylethylamine. In addition to this, Dale took great care in his early work not to suggest that histamine was actually involved in normal physiological processes: “…a possibility that was almost clamouring to be recognized,” in his own words (Dale 1953, p. 337). The statement that histamine played a physiological role in vivo had to await the proof of its existence as a natural component of tissue. This was hinted at by early work (Barger and Dale 1911; Abel and Kubota 1919) but was not shown conclusively until 1927 (Best et al. 1927). By 1929, in his Croonain Lectures, Dale readily acknowledged that histamine was a normal constituent of many tissues (Dale 1929).
