Endostatin inhibits bradykinin-induced cardiac contraction

被引:6
|
作者
Yasuda, Jumpei [1 ]
Takada, Lila [1 ]
Kajiwara, Yuka [1 ]
Okada, Muneyosi [1 ]
Yamawaki, Hideyuki [1 ]
机构
[1] Kitasato Univ, Sch Vet Med, Lab Vet Pharmacol, Higashi 23 Bancho 35-1, Towada, Aomori 0348628, Japan
来源
JOURNAL OF VETERINARY MEDICAL SCIENCE | 2015年 / 77卷 / 11期
关键词
bradykinin; bradykinin type 2 receptor; endostatin; voltage-dependent calcium channel; RECEPTOR; HEART; PROLIFERATION; ANGIOGENESIS; EXPRESSION; MIGRATION; K.ACH;
D O I
10.1292/jvms.15-0200
中图分类号
S85 [动物医学(兽医学)];
学科分类号
0906 ;
摘要
Endogenous fragments of extracellular matrix are known to possess various biological effects. Levels of endostatin, a fragment of collagen type XVIII, increase in certain cardiac diseases, such as cardiac hypertrophy and myocardial infarction. However, the influence of endostatin on cardiac contraction has not been clarified. In the present study, we investigated the effects of endostatin on bradykinin-induced atrial contraction. Isometric contractile force of mouse isolated left atria induced by electrical current pulse was measured. Voltage dependent calcium current of guinea pig ventricular myocytes was measured by a whole-cell patch-clamp technique. Endostatin (100-1,000 ng/ml) alone treatment had no influence on left atrial contraction. On the other hand, pretreatment with endostatin (300 ng/ml) significantly inhibited bradykinin (1 mu M)-induced contraction and voltage-dependent calcium current. These data suggest that endostatin may decrease bradykinin-induced cardiac contraction perhaps through the inhibition of voltage-dependent calcium channel.
引用
收藏
页码:1391 / 1395
页数:5
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