M. Nishimura et al., SODIUM-INTAKE REGULATES RENIN GENE-EXPRESSION DIFFERENTLY IN THE HYPOTHALAMUS AND KIDNEY OF RATS, Journal of hypertension, 15(5), 1997, pp. 509-516
Objective To elucidate the different effects of sodium intake on renin
messenger RNA (mRNA) in the hypothalamus and the kidney and to invest
igate the role of hypothalamic renin in sodium-induced hypertension, D
esign and methods We investigated the expression of the renin gene in
the hypothalamus and the kidney of rats with altered sodium intake and
those administered either deoxycorticosterone acetate (DOCA) or sodiu
m, Diets containing a high (8% NaCl), normal (2% NaCl), or low (0.2% N
aCl) amount of sodium were administered to 12-week-old male Wistar rat
s for 10 days or 8 weeks before the rats were killed, Male Wistar rats
administered either DOCA or 1% NaCl were killed 2 weeks (during the p
rehypertensive stage) or 6 weeks (during the hypertensive stage) after
the start of treatment, The hypothalamus and kidneys were excised for
extraction of total RNA, Competitive polymerase chain reaction of ren
in mRNA and deletion-mutated renin RNA was performed, and the renin mR
NA concentration was calculated, Results A high sodium intake for 10 d
ays increased the renin mRNA in the hypothalamus; the hypothalamic ren
in mRNA had not been suppressed after 8 weeks of a high sodium intake
despite the lowering in renal renin mRNA. Renin mRNA levels in the hyp
othalamus were not suppressed either in the prehypertensive or in the
hypertensive stage in rats treated with DOCA or sodium, or both, altho
ugh the renal renin mRNA was reduced in rats administered DOCA or sodi
um, or both, compared with that in sham-treated control rats, during b
oth stages, Conclusions The expression of the renin gene is regulated
differently in the rat hypothalamus from that in the kidney, The const
ant expression of the renin gene in the hypothalamus during a chronic
high sodium load might be related at least in part to the mechanism of
the activated brain renin-angiotensin system in sodium-induced hypert
ension.