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Relationship between Urinary Kallikrein and Renal Sodium Handling during Water Immersion in Normal Man^*

Medical and Research Services, Veterans Administration Medical Centers Miami, Florida 33125 Medical and Research Services, Veterans Administration Medical Centers San Diego, California 92161 The Departments of Medicine, University of Miami School of Medicine Miami, Florida 33125 The University of California, San Diego, School of Medicine San Diego, California 92161

Address requests for reprints to: Murray Epstein, M.D., Nephrology Section 111C1, Veterans Administration Medical Center, 1201 Northwest 16th Street, Miami, Florida 33125.

Considerable controversy exists with regard to the physiological role of the renal kallikrein-kinin system in regulating renal sodium handling. It has been both suggested and denied that a positive relationship exists between urinary sodium excretion and kallikrein activity. This discrepancy may relate in part to the experimental manipulations used to achieve extracellular fluid volume expansion, since the infusion of exogenous solutions is frequently accompanied by alterations in plasma composition and urine flow which may affect the kallikrein- kinin system independently of volume alterations. The successful characterization of the water immersion model (NI) and the demonstration that it induces acute central hypervolemia without concomitant alterations in plasma composition commended its utilization in the present study. The NI model was used to assess in a kinetic fashion the relationship between urinary kallikrein excretion and renal sodium handling. Normal subjects were studied after 11 h of dehydration on two occasions: control (C; 7 studies) and during 4 h of NI (6 studies). Urinary sodium, potassium, and kallikrein excretion were measured hourly. NI was associated with a marked increase in urinary Na excretion [from 70 ± 15 to 206 ± 18 (SE) µeq/min; P < 0.005]. Concomitantly, urinary kallikrein excretion was unchanged. The current demonstration that NI failed to augment kallikrein excretion despite the marked concomitant natriuresis is consistent with the formulation that the kallikrein-kinin system may not participate in the acute regulation of sodium homeostasis in man.

^* This work was supported in part by designated V.A. Research Funds and grants from the National Aeronautics and Space Administration (NAS 9-15473) and the NIH (HL-18095).

Received May 18, 1979.