Kallikrein excretion in Dahl salt-sensitive and salt-resistant rats with native and transplanted kidneys

Urinary kallikrein excretion is decreased in Dahl salt-sensitive (S) vs. salt-resistant (R) rats, and several lines of reasoning suggest not only that decreased kallikrein excretion is a marker for salt-sensitive hypertension but also that kallikrein might play a pathogenic role. Because previous cross-transplantation studies have demonstrated that the kidney's genotype plays a role in determining the blood pressure of the recipient in Dahl S and R rats, the present experiments were designed to determine whether both blood pressure and urinary kallikrein excretion "traveled with the kidney" in transplantation. The Rapp strains of S and R were maintained on a low- NaCl (0.13%) diet until kidney transplantation (bilaterally nephrectomized recipients), at which time the diet was switched to high NaCl (7.8%). Sixteen days later, blood pressures (tail-cuff plethysmography) of the cross-transplant groups (R/S and S/R, indicating kidney genotype/recipient genotype) were nearly identical to each other and intermediate between the blood pressures of the control groups with transplanted kidneys (R/R and S/S). Renal function studies, performed on anesthetized rats 17 days after surgery, demonstrated that R kidneys had higher glomerular filtration rates, renal plasma flows, and urinary kallikrein excretion rates than S kidneys. These differences tended to be preserved in the cross-transplant groups, and therefore they must be genetically determined intrinsic differences between R and S kidneys. This was especially striking with respect to urinary kallikrein excretion. The rank order of urinary kallikrein excretion was R/R = R/S > S/R = S/S, which implies that it is completely determined by the genotype of the kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Gender Differences in Urinary Kallikrein Excretion in Man: Variation Throughout the Menstrual Cycle

1. Urinary kallikrein excretion was measured in healthy male subjects and in healthy pre- and post-menopausal females. 2. Urinary kallikrein excretion was shown to be constant throughout a 24 h period. Individual male subjects showed little fluctuation in urinary kallikrein excretion; within-subject variance accounted for 1.65% of the total. 3. Female subjects with ovulatory menstrual periods excreted significantly more kallikrein than post-menopausal females and males. 4. Pre-menopausal females showed a much greater within-subject variation in urinary kallikrein excretion and this could be related to the stage of the menstrual cycle, with significantly greater urinary kallikrein excretion in the luteal phase than in the follicular phase. 5. Plasma renin activity and plasma aldosterone concentration also showed a menstrual variation, with concentrations in the luteal phase being significantly higher than those in the follicular phase. 6. The rise in urinary kallikrein excretion in the luteal phase could be abolished by oral administration of the aldosterone antagonist spironolactone. 7. Urinary kallikrein excretion in post-menopausal females was similar to the range found in males, and showed no cyclic changes over a 4 week period. 8. Gender and menstrual status should be taken into account in studies of the physiological role of tissue kallikreins.