Effect of Candesartan on high-salt induced ventricular hypertrophy and the expression of inflammatory cytokines.doc
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Effect of Candesartan on high-salt induced ventricular hypertrophy and the expression of inflammatory cytokines
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Effect of Candesartan on high-salt induced ventricular hypertrophy and the expression of inflammatory cytokines
[Abstract] Objective of angiotensin 1 receptor (AT1R antagonist in high-salt diet rats and ventricular hypertrophy and inflammatory factor expression. Methods 30 Wistar rats were randomly divided into high-salt group, high salt + candesartan treatment group (2 mg / kg / d, high salt + triple intervention group (mg / kg / d: 20 hydralazine + 7 hydrochlorothiazide + 0.15 reserpine, n = 10. The groups were 8% NaCl high salt pellets fed in the intervention group were to triple drug candesartan or orally., respectively, before the experiment, experiment, and 8 w 4 w after the end of arterial blood pressure measured, 8 w later known as left ventricular weight (LVM), calculated left ventricular / body mass index (LVI), using enzyme-linked immunosorbent assay (ELISA measured serum interleukin-1 (IL 1, interleukin 6 (IL 6 expression. Results high-salt diet for 8 w, the high salt group compared with baseline blood pressure was significantly higher (P lt;0.01, candesartan or triple salt and high blood pressure drug intervention group were significantly decreased (all P lt;0.01, and the two groups no significant difference in blood pressure in the intervention group ( Pgt; 0.05). candesartan group LVM reduce high salt group, LVI lower (P lt;0.01), while the triple therapy group, although reduced but did not reach statistical significance (Pgt; 0.05. candesartan group high salt group or the triple therapy group had significant IL 1, IL 6 expression decreased (all P lt;0.01), while the triple therapy group and the high salt group showed no significant difference (Pgt; 0.05). Conclusion fed high salt can lead to cardiac hypertrophy, is not entirely dependent on the increase in blood pressure. AT1R antagonist can reverse the cardiac effects of high salt, independent of the antihypertensive effect beyond its anti-inflammatory effects.
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