Key result
Co-administration of aprotinin increased the natriuretic and diuretic effects of atrial natriuretic factor by 50% in rats, suggesting glandular kallikrein may be involved in ANF catabolism.
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Hypothesis-generating for kallikrein in ANF catabolism; human studies required before clinical consideration.
The rat atrium contains a potent natriuretic factor which appears to inhibit the sodium reabsorption in the collecting tubules of the kidneys. We examined the effects of the injection of partially purified atrial natriuretic factor (ANF) and synthetic ANF (8-33) into rats with simultaneous infusions of dextrose or aprotinin. Aprotinin, an inhibitor of serine proteases, increases the natriuretic and diuretic effects of the atrial factor by 50%. Urinary kallikrein excretion is also slightly increased by ANF but is not affected by aprotinin. As a comparison, aprotinin has no effect on the diuretic or natriuretic responses of furosemide, although it inhibits by 50% the kallikrein excretion induced by furosemide. When ANF is incubated with purified rat urinary kallikrein, the natriuretic and diuretic effects are decreased by more than 50%. We conclude that glandular kallikrein or a similar serine protease may be involved in the catabolism of ANF.
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Thibault et al. (1984) studied this question. Atrial natriuretic factor (ANF) and aprotinin vs. ANF and dextrose was evaluated on Natriuretic and diuretic effects. Co-administration of aprotinin increased the natriuretic and diuretic effects of atrial natriuretic factor by 50% in rats, suggesting glandular kallikrein may be involved in ANF catabolism.
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