机械敏感阳离子通道介导离体大鼠肾脏入球小动脉的肌源性收缩。
Mechanosensitive cation channels mediate afferent arteriolar myogenic constriction in the isolated rat kidney.
作者信息
Takenaka T, Suzuki H, Okada H, Hayashi K, Kanno Y, Saruta T
机构信息
Department of Medicine, Saitama Medical College, Iruma, Saitama 340-03, Japan.
出版信息
J Physiol. 1998 Aug 15;511 ( Pt 1)(Pt 1):245-53. doi: 10.1111/j.1469-7793.1998.245bi.x.
Abstract
- In order to assess ionic mechanisms mediating renal afferent arteriolar myogenic constriction, experiments were performed using isolated perfused hydronephrotic rat kidneys. 2. Increasing pressure progressively constricted the afferent arteriole (-0.26 +/- 0.02% mmHg-1, n = 21, r = 0.97). Gadolinium (10 microM), a mechanosensitive cation channel blocker, abolished this myogenic constriction. However, high potassium media (30 mM) constricted the afferent arteriole in the presence of gadolinium. 3. Lowering extracellular sodium concentration gradually attenuated afferent arteriolar myogenic constriction. In the perfusate containing 50 mM sodium, the myogenic response was arrested. 4. Afferent arteriolar myogenic constriction was prevented in calcium-free perfusate or by the L-type calcium channel blocker diltiazem (10 microM). 5. Our present findings provide evidence that increasing pressure gates mechanosensitive cation channels on the afferent arteriole, thereby eliciting membrane depolarization and activating voltage-dependent calcium channels.
摘要
- 为了评估介导肾入球小动脉肌源性收缩的离子机制，我们使用离体灌注的肾积水大鼠肾脏进行了实验。2. 压力增加会使入球小动脉逐渐收缩（-0.26±0.02% mmHg-1，n = 21，r = 0.97）。机械敏感阳离子通道阻滞剂钆（10 microM）可消除这种肌源性收缩。然而，在存在钆的情况下，高钾培养基（30 mM）会使入球小动脉收缩。3. 降低细胞外钠浓度会逐渐减弱入球小动脉的肌源性收缩。在含有50 mM钠的灌注液中，肌源性反应停止。4. 在无钙灌注液中或使用L型钙通道阻滞剂地尔硫䓬（10 microM）可防止入球小动脉的肌源性收缩。5. 我们目前的研究结果表明，压力增加会打开入球小动脉上的机械敏感阳离子通道，从而引发膜去极化并激活电压依赖性钙通道。
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