The study provides evidence for the existence of inactive renin in the rat brain, suggesting that the brain renin-angiotensin system may be modulated by the conversion of inactive to active renin.
Offers no clinical implications; leaves open whether inactive renin conversion modulates brain RAS regulation.
Inactive renin in rat brains was investigated according to the following experiments. Treatment with either trypsin or glandular kallikrein of the brain tissue caused a rapid and apparent increase in the renin activity at either 0 or 27 degrees C. The molecular weight of the active renin was estimated to be 40,000 daltons, while that of the trypsin-activatable inactive renin was found to be 48,000 or 61,000 daltons on a column chromatography with Sephadex G-100. The contents of the active renin was the highest in the hypothalamus, followed by striatum, thalamus, midbrain, cerebral cortex, medulla oblongata and cerebellum, while the contents of the trypsin-activatable inactive renin was the highest in the hypothalamus, followed by striatum, thalamus, midbrain, cerebellum, cerebral cortex and medulla oblongata. These results suggest that inactive renin(s) exist in the brain. It seems likely that the brain renin-angiotensin system is modulated by the conversion of inactive to active renin(s).
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Mizuno et al. (1984) studied this question.
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