Decreased urinary active and inactive kallikrein by chronic infusion of vasopressin in conscious rats.

Abstract

To assess possible interactions of circulating vasopressin with the synthesis or activation of renal kallikrein, we studied the effect of chronic infusion of vasopressin (7.2 U/kg/day i.p.) for 6 days on the urinary excretion of total and active kallikrein in conscious rats. We determined urinary total, active and inactive kallikrein by measuring kallikrein activity using a kininogenase assay before and after the treatment with trypsin (200pg/ml). Chronic infusion of vasopressin induced sustained decreases in urinary total, active and inactive kallikrein excretion, but did not affect the ratio of active to total kallikrein. The infusion of vasopressin induced significant increases in circulating levels of vasopressin (248.1± 35.2 pg/ml in vasopressin-infused rats (n = 7) compared to 95.5± 14.6 pg/ml in vehicle-infused rats (n = 7), p <0.001) and in weight gain (39.6± 1.3 g in vasopressin-infused rats (n = 7) compared to 29.1 ± 3.3 g in vehicle-infused rats (n = 7), p <0.05), and also sustained decreases in water intake and urine volume, but it did not induce any change in urinary sodium excretion. Circulating levels of angiotensin II was decreased by chronic infusion of vasopressin. Thus, the present study suggests that the elevation of circulating vasopressin levels induces a decrease in the synthesis of renal kallikrein. total kallikrein ; trypsinactivated kallikrein ; renal kallikrein system ; antidiuretic hormone Kallikrein is a serine protease which is synthesized by the kidney and excreted in the urine (Nustad et al. 1975). It liberates kinins, potent vasodilator peptides, from its natural substrate kininogen. Several previous studies have examined the response of urinary kallikrein excretion to altered water metabolism and infused vasopressin in experimental animals and humans (Levinsky 1979;Carretero and Scicli 1980). Previously we have also shown that the infusion of Med

Low-dose vasopressin infusion results in increased mortality and cardiac dysfunction following ischemia-reperfusion injury in mice

“…Intraperitoneal pumps (1 μL/hour for 72 hours, Alzet micro-osmotic pump, Alza Corporation, Palo Alto, CA, USA) delivered normal saline (SL control), DOB at 8.33 μg/kg/minute, or arginine vasopressin at 0.00057 Units/kg/minute (equivalent to 0.04 Units/minute in a 70 kg human; AVP treatment). AVP levels in rodents and humans are similar, while in rodents the intraperitoneal route of administration for AVP increases plasma AVP levels in a manner very similar to intravenous dosing in humans [ 34 , 35 ]. At least five mice per time point in each group were studied.…”