[Mechanism of urinary output inhibited by Vitamin D analogs in mice]

To explore the effect of vitamin D analogs regulated mice urinary output on depressed expression of renin-angiotensin in paraventricular nucleus.

A total of 51 C57BL/6 mice were randomly divided into control (n = 36) and vitamin D receptor knockout (VDR, n = 15) groups. Then the tests of water deprivation, vitamin D analogue injection and 0.25% captopril water drinking were performed. Renin levels in paraventricular nucleus and plasma and aquaporin in kidney were determined by immunofluorescence, real-time polymerase chain reaction (PCR) and Western blot.

The urinary output of VDR knockout mice decreased markedly after 48 h water deprivation [(129 ± 45 vs 1 354 ± 224) ml/24 h, P < 0.05] while there was little change of urinary and plasma osmolarity. The expression levels of AQP-4 and rennin in VDR knockout mice were higher than those of wild type. Renin and angiotensin II in periventricular nucleus of VDR knockout mice were higher than those of wild type and was reduced by injecting vitamin D analogs into wild type. Rennin activity: (139 ± 31 vs 185 ± 56) mcU/ml; angiotensin II: (33 ± 32 vs 72 ± 27) pg/ml, (both P < 0.05). There was statistically significant differences. The expression of c-fos in periventricular nucleus in VDR knockout mice was higher and it could be inhibited after an injection of vitamin D analog.

Thirsty in central nervous system is inhibited by vitamin D analogs through reduced renin-angiotensin activity in paraventricular nucleus. Polydipsia and polyuria may be caused by a lack of vitamin D. Captopril lowers urinary output.