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Prophylactic effects of an N- and L-type Ca2+ antagonist, cilnidipine, against cardiac hypertrophy and dysfunction in stroke-prone, spontaneously hypertensive rats

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Abstract:

To clarify the beneficial effects of cilnidipine, an L- and N-type calcium channel blocker, which were clinically observed against diastolic dysfunction in hypertrophied hearts of hypertensive patients, we investigated the effects of cilnidipine on cardiac remodeling and enhanced gene expression in stroke-prone, spontaneously hypertensive rats in comparison with that of captopril, a well-known angiotensin-converting enzyme inhibitor, at threshold doses with little blood pressure lowering effect. The expression of type III collagen and /α-myosin heavy chain as well as transforming growth factor-, and basic fibroblast growth factor were suppressed by both treatments, indicating the prevention or amelioration of cardiac dysfunction. Such beneficial effects were much more intense with cilnidipine treatment than in captopril. These results indicate that Ca2+ is a key factor in the pathogenesis of cardiac remodeling in hypertension. One possible beneficial effect of cilnidipine in the prevention of cardiac dysfunction may be due to the decreased amount of growth factors such as transforming growth factor- and basic fibroblast growth factor via direct action for Ca2+ influx and also via inhibition of local renin-angiotensin system in the myocardium.Key words: hypertension, cardiac hypertrophy, Ca2+-blocker, growth factor.

Les effets bénéfiques de la cilnidipine, un bloqueur des canaux calciques de type L et N, sur la dysfonction diastolique ont été observés en clinique dans les cœurs hypertrophiés de patients hypertendus. Afin de clarifier ces effets, nous les avons examinés sur le remodelage cardiaque et l'augmentation de l'expression génique chez des rats spontanément hypertendus prédisposés aux accidents vasculaires cérébraux, et nous les avons comparés à ceux du captopril, un inhibiteur bien connu de l'enzyme de conversion de l'angiotensine, à des doses seuils ayant un effet hypotenseur négligeable. Les deux traitements ont supprimé l'expression du collagène de type III et de la chaîne lourde de /α-myosine, du facteur de croissance transformant  (TGF-) et du facteur de croissance basique des fibroblastes (bFGF), une indication de prévention ou de diminution de la dysfonction cardiaque. Ces effets bénéfiques ont été plus prononcés avec le traitement à la cilnidipine qu'avec le traitement au captopril. Ces résultats indiquent que le calcium (Ca2+) est un facteur clé dans la pathogenèse du remodelage cardiaque durant l'hypertension. Un des effets possibles de la cilnidipine dans la prévention de la dysfonction cardiaque pourrait découler de la diminution du taux de facteurs de croissance, tels que TGF- et bFGF, par une action directe sur l'entrée de Ca2+ de même que par une inhibition du système rénine-angiotensine local dans le myocarde.Mots clés : hypertension, hypertrophie cardiaque, bloqueur de Ca2+, facteur de croissance.[Traduit par la Rédaction]

Document Type: Research Article

Publication date: August 1, 2005

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