A series of observations haveLeen made recently, the resultscf which suggest, a relationship between arterial hypertension and guanidine metabolism. Major and Stephenscn (1) studyipg the influence of certain urinary constituents on blood pressure, noted that methyl guanidine, a product of normal metabolism and a constituent of normal urine, had marked pressor effects. These authors suggested that this compound, if produced in excess or imperfectly excreted, might account for increased blood pressure. Creatinine and creatine, substances closely allied to methyl guanidine chemically, were found inert. Later (2) observations confirmed the rise in blood pressure following experimental injection of methyl guanidine. In addition it was then noted that, in short period experiments, rise in blood pressure produced by guanidine compounds could be abolished by the use of calcium or potassium chloride. The latter is of interest, in view of the clinical results obtained from the use of these salts as reported by Addiscn (3) and Addison and Clark (4), who found that these inorganic salts, when given in large doses (about 15 grams per day) over long periods of time, produced a diuresis and accompanying this there was a decided and prolonged fall in blood pressure in a large percentage of cases of hypertension. In a further communication Major (5) reported two cases of arterial hypertension. in which the daily excretions of guanidine bases were observed. In both, during produced diuresis, a rise in urinary excretion of dimethyl-guanidine was acccmpanied by a fall in blood pressure. Experimental evidence was also presented by the same worker (6) favoring the view that the elevation in blocd pressure 587

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