It is well known that the normal kidney "escapes" the sodium retaining effect of mineralocorticoids. However, the mechanism that mediates this "escape" is not understood. The possible role of kallikrein in this "escape" phenomenon was investigated by placing seven dogs in metabolic cages and giving them a constant sodium diet. After they had been on this diet three days, urine was collected for two 24-hour periods. DOCA (25 mg/day) was then given intramuscularly for five days. Urine was collected daily during this DOCA period and for two additional 24- hour periods. Urine volume, sodium, potassium, protein, and kallikrein excretion were then measured. Urinary kallikrein increased from 251.9 ± 34.8 (mean ± SE) in the second day of the control period to 639.8 ± 110.1 IJ-g/day (P < .01) by the third day of treatment. It remained elevated two days after DOCA was discontinued. Sodium excretion decreased significantly on the first day of DOCA treatment, returning to the previous values thereafter. Urine protein excretion remained constant. The enhanced urinary kallikrein during the "escape" suggests that the kallikrein system could be involved in the regulation of sodium metabolism by acting as a natriuretic factor, or perhaps by regulating the renal blood flow.
Marin-Grez, M.; Oza, N. B.; and Carretero, O. A.
"The Involvement of Urinary Kallikrein in the Renal Escape from the Sodium Retaining Effect of Mineralocorticoids,"
Henry Ford Hospital Medical Journal
: Vol. 21
Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol21/iss2/5