Activation of renal outer medullary potassium channel in the renal distal convoluted tubule by high potassium diet / 生理学报

Renal outer medullary potassium (ROMK) channel is an important K+ excretion channel in the body, and K+ secreted by the ROMK channels is most or all source of urinary potassium. Previous studies focused on the ROMK channels of thick ascending limb (TAL) and collecting duct (CD), while there were few studies on the involvement of ROMK channels of the late distal convoluted tubule (DCT2) in K+ excretion. The purpose of the present study was mainly to record the ROMK channels current in renal DCT2 and observe the effect of high potassium diet on the ROMK channels by using single channel and whole-cell patch-clamp techniques. The results showed that a small conductance channel current with a conductance of 39 pS could be recorded in the apical membrane of renal DCT2, and it could be blocked by Tertiapin-Q (TPNQ), a ROMK channel inhibitor. The high potassium diet significantly increased the probability of ROMK channel current occurrence in the apical membrane of renal DCT2, and enhanced the activity of ROMK channel, compared to normal potassium diet (P < 0.01). Western blot results also demonstrated that the high potassium diet significantly up-regulated the protein expression levels of ROMK channels and epithelial sodium channel (ENaC), and down-regulated the protein expression level of Na+-Cl- cotransporter (NCC). Moreover, the high potassium diet significantly increased urinary potassium excretion. These results suggest that the high potassium diet may activate the ROMK channels in the apical membrane of renal DCT2 and increase the urinary potassium excretion by up-regulating the expression of renal ROMK channels.

Study on protective effect of vitamin E for ovarian grandlose cells and its mechanism in aged rats / 中国应用生理学杂志

<p><b>AIM</b>To observe the effect of vitamin E (VE) on ovarian apoptosis-related protein Bcl-2 and Bax and its impact on antioxidant capacity in aged female rats and to study the senility-delaying effect and mechanism of VE on ovary.</p><p><b>METHODS</b>Natural aging female rats were given different doses of exogenous VE. Then apoptosis regulatory protein Bcl-2, Bax expression in ovarian grandlose cells were detected by using immunohistochemical methods and Western blot. The contents of serum total superoxide dismutase (SOD) activity and malondialdehyde (MDA) were detected by using biochemical methods.</p><p><b>RESULTS</b>Contrasted with adult control group, the level of Bcl-2 expression in Senile control group was lower and the level of Bax expression was higher (P < 0.01), Serum SOD activity decreased and the level of MDA significantly increased (P < 0.01). Contrasted with senile control group, the level of Bcl-2 expression increased in VE group, the level of Bax expression decreased (P < 0.05), the level of MDA expression significantly decreased (P < 0.01).</p><p><b>CONCLUSION</b>VE can regulate apoptosis-related protein Bcl-2, Bax expression and confront free radical damage which contribute to a protective effect for ovarian grandiose cells.</p>

Effects of vitamin E on expression of PS-1 and production of Abeta in the hippocampus of female senile rats / 中国应用生理学杂志

<p><b>AIM</b>To observe the expression of Presenilin-1 (PS-1) and production of amyloid beta-protein (Abeta) in hippocampus of female senile rats and to investigate the effect of vitamin E(VE) on preventing Alzheimer's disease after menopause.</p><p><b>METHODS</b>The animal model was established using female senile rats. Experimental groups (n=8) were respectively given different doses of VE(5 mg/kg, 15 mg/kg, 60 mg/kg) per day. The expression of PS-1 in hippocampus was detected by immunohistochemistry, the level of Abeta in hippocampus was measured by Radioimmunoassay, and neuronal ultrastructure in hippocampal DG area was observed using transmission electron microscope.</p><p><b>RESULTS</b>The expression of PS-1 in rat hippocampus of senile control group was stronger than that of adult control group. PS-1 expressed weakly in three medication groups along with augmentation of dosage. The levels of Abeta were found to correlate statistically with the expression of PS-1. The content of Abeta in VE groups was significantly decreased compared to that in senile control group (P < 0.01). There were some changes in the neuronal ultrastructure of senile rats. Neurons were gradually recovered in VE groups.</p><p><b>CONCLUSION</b>VE may depress the production of Abeta by regulating the expression of PS-1, reducing neuronal injuries. VE may play a role in neuronal protection.</p>