1. Urinary kallikrein excretion in the anaesthetized rat was measured during intravenous KCl infusion in control and in K + -adapted rats. 2. The infusion of 0.1 mol/l KCl at 3.0 ml/h for 60 min in control rats resulted in a significant increase in urinary kallikrein excretion, associated with diuresis, natriuresis and kaliuresis. 3. When rats were offered 0.1 mol/l KCl to drink ad libitum for 14 days (K + -adaptation), the basal excretion of kallikrein was higher than in the control rats. In K + -adapted rats, intravenous infusion of 0.1 mol/l KCl resulted in significantly greater increase in urinary kallikrein excretion than in the control rats. 4. The Na + -channel blocker, amiloride (8.5 mg/kg body weight), significantly increased urinary kallikrein excretion immediately after injection in control and K + -adapted rats. However, in the subsequent 60 min, kallikrein excretion decreased markedly to values lower than those before injection of amiloride. 5. When amiloride was superimposed on a continuous 0.1 mol/l KCl infusion in K + -adapted rats, there was an immediate increase in kallikrein excretion. In the subsequent 20 min, kallikrein excretion decreased only to increase again in the next 40 min of KCl infusion. 6. Since amiloride injection reduces urinary kallikrein excretion in control and K + -adapted rats, the results suggest that urinary kallikrein excretion in the rat is through a mechanism(s) affected by amiloride. The high urinary kallikrein excretion and the greater response to KCl infusion in K + -adapted rats suggest that the K + -transport mechanism is more important than the mechanism affected by amiloride.

1. The cardiovascular effects of pressor doses of arginine vasopressin were examined in anaesthetized Brattleboro rats with hereditary diabetes insipidus (BDI) and normal rats of the parent Long Evans (LE) strain, either 37 or 85 days old. 2. Control mean arterial blood pressure and total peripheral resistance were similar in adult animals of the two strains but were significantly lower in the young BDI rats compared with the young LE rats. 3. The three doses of vasopressin produced greater pressor responses in the young, immature LE rats compared with the young BDI rats, whereas in the adult animals vasopressin had the greater pressor effect in the BDI rats compared with the LE rats of comparable age. 4. There was little effect of vasopressin on cardiac output after the initial decrease, particularly in the BDI rats whether immature or adult, despite more prolonged decreases in heart rate. 5. These studies indicate important age-related differences in the pressor response to vasopressin in anaesthetized rats, in addition to the clear differences in response between the animals with (LE) or without (BDI) the circulating endogenous peptide.

1. The effect of amiloride administration on the urinary kallikrein response to the injection or continuous infusion of frusemide in normal Sprague–Dawley rats was investigated. 2. Injections of frusemide induced repeatedly an increase in urinary kallikrein excretion. This effect was suppressed by amiloride. Amiloride also blocked the response to mannitol injection. A continuous infusion of frusemide lasting 100 min also induced an increase in urinary kallikrein excretion which persisted throughout the experiment. This response was completely blocked by the injection of amiloride. 3. Urinary kallikrein excretion was directly and positively related to urine volume and urinary sodium excretion before and after amiloride injection. The regression lines had markedly decreased slopes after amiloride administration. The urinary kallikrein excretion was also positively related to the urine volume and urinary sodium excretion when frusemide was continuously infused. However, these relationships were abolished after amiloride injection. 4. In both the injection and the infusion experiments, there was a direct relationship of urinary kallikrein excretion to urinary potassium excretion. Although this relationship persisted after amiloride injection, the regression line was shifted to the left. 5. The suppression of the kallikrein stimulating effect of frusemide by the sodium channel blocker amiloride indicates that distal tubule sodium re-absorption is the triggering factor in urinary kallikrein excretion. The study suggests that the mechanism involved in the release of kallikrein by the distal tubular cells is linked to the renal mechanism affected by amiloride.

1. The effect of repeated intravenous injections of frusemide (0.17 mg/kg) on the urinary kallikrein excretion of normal, adrenalectomized and deoxycorticosterone acetate (D0CA)-treated adrenalectomized rats was studied. 2. Adrenalectomy decreased baseline urinary kallikrein excretion, while DOCA treatment restored it to normal. 3. Frusemide injections repeatedly increased urinary kallikrein excretion in the three groups of rats studied. Compared with control and DOCA-treated animals, adrenalectomized rats were less responsive. 4. The excretion of urinary kallikrein was positively correlated with urine volume and with the excretion of sodium and potassium in all groups. The regression lines were shifted to the left in DOCA-treated adrenalectomized rats showing that mineralocorticoids enhance the effect of frusemide on urinary kallikrein excretion. The regression lines between urinary kallikrein excretion and the measured variables in adrenalectomized rats did not differ from those of control animals. 5. We conclude that the response of urinary kallikrein to frusemide is influenced by the level of mineralocorticoid activity. The effect of frusemide on urinary kallikrein excretion does not appear to be a ‘wash-out’ of the enzyme since its influence did not subside after repeated injections.

1. The influence of dietary sodium intake on the pressor response to intravenously infused dopamine in the conscious rat was studied. 2. Chronic sodium restriction significantly reduced the pressor response to infused dopamine, whereas high sodium diet enhanced the response. 3. Sodium intake is an important determinant of the pressor response to dopamine.