Tsubokou Yusuke, Kobayashi Naohiko, Mita Shin-ichiro, Yoshida Kohtaro, Matsuoka Hiroaki
Department of Hypertension and Cardiorenal Medicine, Dokkyo University School of Medicine, Mibu, Tochigi 321-0293, Japan
Eur J Pharmacol. 2002 Dec 20;457(2-3):85-93. doi: 10.1016/s0014-2999(02)02648-1.
We evaluated the cardioprotective effects of long-term treatment with celiprolol (for 5 weeks), a specific beta(1)-adrenoceptor antagonist with a weak beta(2)-adrenoceptor agonist action, on endothelin-1 and transforming growth factor (TGF)-beta(1) expression and cardiovascular remodeling in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Upregulated preproendothelin-1, endothelin ET(A) receptor, TGF-beta(1), c-fos, and type I collagen expression and extracellular signal-regulated kinase activities were suppressed by celiprolol. Celiprolol effectively inhibited vascular lesion formation such as medial thickness and perivascular fibrosis. These observations suggested that extracellular signal-regulated kinase and c-fos gene pathway may contribute to the cardiovascular remodeling of DOCA rats, and that cardioprotective effects of celiprolol on cardiovascular remodeling may be mediated, at least in part, by suppressed expression of endothelin-1 and TGF-beta(1).
我们评估了塞利洛尔(为期5周)长期治疗对醋酸脱氧皮质酮(DOCA)-盐高血压大鼠内皮素-1和转化生长因子(TGF)-β1表达及心血管重塑的心脏保护作用。塞利洛尔是一种具有弱β2肾上腺素能受体激动作用的特异性β1肾上腺素能受体拮抗剂。塞利洛尔可抑制前内皮素-1、内皮素ET(A)受体、TGF-β1、c-fos和I型胶原表达上调以及细胞外信号调节激酶活性。塞利洛尔有效抑制了血管病变形成,如中层厚度和血管周围纤维化。这些观察结果表明,细胞外信号调节激酶和c-fos基因途径可能参与了DOCA大鼠的心血管重塑,并且塞利洛尔对心血管重塑的心脏保护作用可能至少部分是通过抑制内皮素-1和TGF-β1的表达来介导的。