Urinary kallikrein excretion was measured in 21 healthy subjects and 44 patients with various types of hypertension.The kallikrein activity was determined by the method of esterolytic assay. The excretion rates in normal subjects were 112.9•}11.1 (S.E.) EU/day.The kallikrein excretion was decreased in patients with essential hypertension, the mean estimated values were 75.2•}10.0 EU/day. In this disease, however, an enhancement of urinary kallikrein was observed after sodium depletion.An obvious increase in kallikrein excretion was found in the primary aldosteronism.In primary aldosteronism and renovascular hypertension, one of the secondary aldosteronisms, there was a good correlation between the urinary kallikrein output and the urinary sodium excretion. The present data indicate that the renal kallikrein-kinin system, one of the renal anti hypertensive factors, is suppressed in essential hypertension and is under the influence of mineralocorticoid levels. -kallikrein esterolytic assay; kallikreinkinin system;various types of hypertensionThe presence of kallikrein in human urine has been known since Frey's original studies (Frey 1926). Urinary kallikrein differ distinctly from the plasma kallikrein (Webster and Pierce 1963) but they are indistinguishable from kidney kallikrein in molecular dimensions, pH optima and inhibitors behaviour (Nustad 1970). It is supposed that urinary kallikrein, produced in the kidney and excreted in urine, might be one of the renal antihypertensive factors. However, studies on the role of kallikrein-kinin system in hypertensive patients have hitherto been very scarce in the literature (Elliot and Nuzum 1934;Miwa 1965). Recently, Margolius and his coworkers (1971, 1972, 1974) described that abnormal excretion of kallikrein was observed in hypertensive patients. These reports attracted much attention of many researchers.In our laboratory, urinary kallikrein excretion was measured in various types of hypertension, and the influence of sodium depletion or sodium load on the urinary kallikrein output was studied in the essential hypertension patients to elucidate the pathophysiological significance of urinary kallikrein in hypertension.

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Male rats more than seven weeks old showed significantly higher activity of hepatic cytosolic glutathione S-transferase (GST) than females. This sex-related difference in GST activities might be explained by the difference in subunit composition of the enzymes between males and females. The relative proportion of subunit composition of GST between adult male and female rats was as follows: Ya, female greater than male; Yb(Yb'), male much greater than female; Yc, female greater than male. Since phenobarbital (60 mg/kg, i.p. for seven days) induced the Yb subunit as well as Ya subunit, the enzyme activity was more increased in males than in females and the sex difference became more marked. 3-Methylcholanthrene (20 mg/kg, i.p. three times) caused an increase of Ya subunit alone, and then the increased extent was greater in females than in males, and resulted in the disappearance of sex difference.

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