Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
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We have prevously reported that, in stroke-prone spontaneously hypertensive rats (SHRSP), salt-load induces cardiovascular hypertrophy and overexpression of prepro-endothelin-1 (prepro-ET-1) that are prevented by lacidipine which protects rats from salt-load related death. The purpose of the present experiments was to further examine salt-dependent expression of genes and the effects of lacidipine. SHRSP (aged 8 weeks) were randomly allocated to salt free (n=10) or 1% NaCl drinking water during 6 weeks with food containing placebo (n=10) or lacidipine for a daily mean intake of 0.3 (n=10) or 1 (n=10) mg/kg. Salt load increased systolic blood pressure (SBP) from 233±5 to 254±6 mmHg and cardiac mass by 17% (P < 0.05). Concomitantly, salt-load increased in heart the abundance of adult and ‘fetal-type' contractile proteins, of type I collagen and of L-type calcium channel gene products, as well as expression of prepro-ET-1 and of TGF-b1 genes examined by Northern blot analysis (P < 0.05). Lacidipine inhibited the salt-related increase of SBP and ventricular mass, and blunted the associated overexpression of ‘fetal-type' contractile proteins, L-type calcium channel, type I collagen, prepro-ET-1 and TGF-b1 (P < 0.05). In conclusion, these results show that lacidipine prevented cardiac remodeling secondary to high salt diet in SHRSP.This indicates that such a prevention is not solely observed with ACE inhibitors.

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Poster Number PA kyselovic0683
Keywords: calcium antagonis, hypertension, cardiac remodelin, salt load, genes expression