目的:探讨桂竹糖芥苷对肾髓袢升支粗段(thick ascending limb,TAL)管周膜50 p S钾通道活性的调控机制。方法:采用细胞贴附式膜片钳技术及免疫印迹技术测定桂竹糖芥苷对50 p S钾通道活性的调控机制。结果:桂竹糖芥苷可明显抑制50 p S钾...目的:探讨桂竹糖芥苷对肾髓袢升支粗段(thick ascending limb,TAL)管周膜50 p S钾通道活性的调控机制。方法:采用细胞贴附式膜片钳技术及免疫印迹技术测定桂竹糖芥苷对50 p S钾通道活性的调控机制。结果:桂竹糖芥苷可明显抑制50 p S钾通道的活性(P<0.01);PKC阻断剂存在时,桂竹糖芥苷不再增加50 p S钾通道的活性(P>0.05)。结论:桂竹糖芥苷可能是通过激活PKC依赖途径抑制50 p S钾通道活性的。展开更多
Renal tubules regulate blood pressure and humoral homeostasis. Mediators that play a significant role in regulating the transport of solutes and water include angiotensin Ⅱ （AngⅡ） and nitric oxide （NO）. AngⅡca...Renal tubules regulate blood pressure and humoral homeostasis. Mediators that play a significant role in regulating the transport of solutes and water include angiotensin Ⅱ （AngⅡ） and nitric oxide （NO）. AngⅡcan signifcantly raise blood pressure via effects on the heart, vasculature, and renal tubules. AngⅡ generally stimulates sodium reabsorption by triggering sodium and fuid retention in almost all segments of renal tu-bules. Stimulation of renal proximal tubule （PT） trans-port is thought to be essential for AngⅡ-mediated hy-pertension. However, AngⅡ has a biphasic effect on in vitro PT transport in mice, rats, and rabbits： stimulation at low concentrations and inhibition at high concentra-tions. On the other hand, NO is generally thought to inhibit renal tubular transport. In PTs, NO seems to be involved in the inhibitory effect of AngⅡ. A recent study reports a surprising fnding： AngⅡ has a mono-phasic stimulatory effect on human PT transport. De-tailed analysis of signalling mechanisms indicates that in contrast to other species, the human NO/guanosine 3’,5’-cyclic monophosphate/extracellular signal-regulat-ed kinase pathway seems to mediate this effect of Ang Ⅱ on PT transport. In this review we will discuss recent progress in understanding the effects of AngⅡ and NO on renal tubular transport.展开更多
文摘目的:探讨桂竹糖芥苷对肾髓袢升支粗段(thick ascending limb,TAL)管周膜50 p S钾通道活性的调控机制。方法:采用细胞贴附式膜片钳技术及免疫印迹技术测定桂竹糖芥苷对50 p S钾通道活性的调控机制。结果:桂竹糖芥苷可明显抑制50 p S钾通道的活性(P<0.01);PKC阻断剂存在时,桂竹糖芥苷不再增加50 p S钾通道的活性(P>0.05)。结论:桂竹糖芥苷可能是通过激活PKC依赖途径抑制50 p S钾通道活性的。
文摘Renal tubules regulate blood pressure and humoral homeostasis. Mediators that play a significant role in regulating the transport of solutes and water include angiotensin Ⅱ （AngⅡ） and nitric oxide （NO）. AngⅡcan signifcantly raise blood pressure via effects on the heart, vasculature, and renal tubules. AngⅡ generally stimulates sodium reabsorption by triggering sodium and fuid retention in almost all segments of renal tu-bules. Stimulation of renal proximal tubule （PT） trans-port is thought to be essential for AngⅡ-mediated hy-pertension. However, AngⅡ has a biphasic effect on in vitro PT transport in mice, rats, and rabbits： stimulation at low concentrations and inhibition at high concentra-tions. On the other hand, NO is generally thought to inhibit renal tubular transport. In PTs, NO seems to be involved in the inhibitory effect of AngⅡ. A recent study reports a surprising fnding： AngⅡ has a mono-phasic stimulatory effect on human PT transport. De-tailed analysis of signalling mechanisms indicates that in contrast to other species, the human NO/guanosine 3’,5’-cyclic monophosphate/extracellular signal-regulat-ed kinase pathway seems to mediate this effect of Ang Ⅱ on PT transport. In this review we will discuss recent progress in understanding the effects of AngⅡ and NO on renal tubular transport.
