Effects of dexamethasone on excretion of urinary kallikrein and urinary protein in Dahl salt-sensitive and salt-resistant rats.
The effect of glucocorticoid treatment on urinary kallikrein excretion was assessed in Dahl salt-hypertension susceptible (S) and salt-hypertension resistant (R) rats. A single dose of dexamethasone (100 micrograms) caused a marked water diuresis and a slight decrease in urinary kallikrein excretion in both S and R rats. A single dose of dexamethasone also caused the S rat to excrete massive amounts of protein into the urine, almost 3-fold higher than S rats treated with oil; the effect on R rat urinary protein was similar, but less severe. Daily administration of dexamethasone (100 micrograms/day) for 7 days caused marked suppression of urinary kallikrein excretion in both S and R rats. Increased urinary protein following chronic treatment was still evident in the dexamethasone-treated S rats but not in the dexamethasone-treated R rats. Chronic glucocorticoid treatment probably inhibits urinary kallikrein activity by suppressing pituitary and adrenal function which would remove the stimulatory effect of aldosterone on urinary kallikrein excretion. There was no evidence for a stimulatory role of glucocorticoids on urinary kallikrein.
D000818:Animals; D003907:Dexamethasone / Q000008:administration & dosage / Q000494:pharmacology*; D004231:Diuresis / Q000187:drug effects; D005260:Female; D006973:Hypertension / Q000139:chemically induced / Q000652:urine*; D007610:Kallikreins / Q000652:urine*; D011507:Proteinuria / Q000652:urine*; D051381:Rats; D012965:Sodium Chloride
D012965:Sodium Chloride; D003907:Dexamethasone; D007610:Kallikreins