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Hypertension, Vol 6, 175-183, Copyright © 1984 by American Heart Association

ARTICLES

Urinary kallikrein response to acute saline or water loads in hypertensive and normal humans

WJ Lawton

Urinary kallikrein excretion during acute water or saline loading was studied in normal and hypertensive humans after chronic Na+ depletion and Na+ loading to answer the following questions. 1. Is urinary kallikrein a natriuretic or diuretic substance? 2. During acute water or saline loading, does the underlying Na+ balance influence (a) the urinary kallikrein response? or (b) the relationship between urinary kallikrein and renal Na+ or water handling? 1) Urinary kallikrein did not change during a 1.2 liter water load given to nine white hypertensive and five white normal men. Urinary kallikrein was significantly decreased, however, in five white hypertensive and five white normal subjects during and after 1 hour of isotonic saline infusion (30 ml/kg). In sodium-depleted hypertensive patients kallikrein excretion was decreased from 19.8 to 9.5 mEU /min, and in Na+-depleted normal subjects it was decreased from 15.7 to 12.6 mEU /min (p = 0.003). The response in hypertensive patients was not different from normal subjects. In all Na+-loaded subjects, kallikrein excretion was also significantly decreased during isotonic saline infusion (p = 0.01). Urinary kallikrein did not change in three other subjects given hypertonic saline. 2(a) The underlying state of Na+ balance influenced the baseline level of kallikrein excretion, but not the directional decline in kallikrein during isotonic saline. (b) In Na+-restricted hypertensives given isotonic saline, urinary kallikrein was inversely related to the fractional excretion of Na+ (r = -0.54, p less than 0.01) and the tubular reabsorption of H2O (TcH2O/GFR; r = - 0.50, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

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