Volume regulated chloride channel (VRCC) enhances cell proliferation through PI3K/Akt signal pathway ,and inhibits cell apoptosis through mitochondrial pathway in vascular smooth muscle cells ,and accelerates the process of atherosclerosis through JNK/p38 MAPK signal pathway,resulting in increasing SR-A expression and ox-LDL uptake. Cerebrovascular remodeling is mediated by VRCC. This effect of VRCC on remodeling is related to accelerating cell proliferation ,migration and accumulation of. extracellular matrix. As to the molecular identification of VRCC ,it is very complex. VRCC is diversity in various cells or tissues , rather than a single ubiquitous channel,VRCC may be contain variedcell type-or tissue-specific subunitcompositions. ClC-3 volume regulated Cl-channel is regulated by both integrin-Src and Rho/RhA-Rock signal pathways.

The effect of the total saponins of panax notogiseng ( PNS ) on transmitter release was studied on mouse diaphragm. The Ca2+ -mediated release evoked by electric stimulation at the nerve terminal or by raised K+ level was markedly reduced by Cd2 + , but not affected by PNS & nifedipine. Also, PNS didn't change the basic frequency of mepp & the Ba2+ entry during depolarization of the terminal. C-ompared with PNS, Cd2 had a significant effect on decreasing Ba2+ entry. These results suggest that PNS can not change spontanous, synchronous or asynchronous release, the Ca2+ channel involved in the transmitter release at the mouse motor nerve terminal belongs in N type Ca2 channel.

Cl - ,ClC 3 chloride current can be inhibited by chloride channel inhibitor DIDS?tamoxifen and extracellular ATP. ClC 3 is modulated by cell volume and regulated by PKC.The present review discusses the expression, eletrophysiology,molecular properties,signal transduction of such channel.

Bestrophins have recently been proposed to comprise a new family of chloride channels.Homologous sequences have been found in animals,fungi and prokaryotes.Bestrophins are regulated by Ca2+,cell volume as well as auto-inhibitory domain and play important roles in olfactory transduction,fluid transport and cell proliferation.

Cerebral vascular diseases throw great threat to human health,among which ischemic stoke accounts for 50%~80%.Rencent results showed that astrocyte can protect the neurons during cerebral ischemia diseases via maintenance extracellular K+ homeostasis,elimination of oxygen free radicals,uptake the excess excitatory amino acid,release of neurotrophic factors and regulation the functions of ion channels.This article reviews the recently published works about the mechanisms of the neuroprotective effects of astrocyte during the cerebral ischemic diseases.

Protein Kinase C-zeta (PKC-?) is a new member of protein kinase C family and has some specific characteristics as comparing with the classical PKC. It lacks the C 2 domain making its kinase activity Ca 2+ -independent, and it possesses only one zinc-finger region in its regulatory domain. Therefore, PKC-? does not bind Ca 2+ and can not be activated by diacylglycerol or phorbol esters. In addition, many researches showed that PKC-? could induce differentiation, mediate insulin-stimulation protein synthesis, activate immunity of human neutrophils, inhibit proliferation of cancer cells and regulate the function of actin cytoskeleton. What is more, PKC-? plays an important role in signal transduction of cells, such as mediating MAPK and NF-?B activation.

Cerebrovascular remodeling is the most important pathologic change during hypertension. Stroke induced by hypertension is threatening thousands of people's lives. The ion channels in cerebrovascular smooth muscle cells may be altered during hypertension and thus the abnormality of cytosolic ion concentration can accelerate cerebrovascular remodeling. These channels, including potassium channels, calcium channels and chloride channels, may play an important role in the cerebrovascular remodeling during hypertension.

Pleiotropic effects of a drug are actions other than that for which the agents were developed.These effects may be desired or undesired,and may be unrelated to their primary mechanism.Statins were designed as a drug for reducing cholesterol,but now pleiotropic effect are found including improvement of endothelial dysfunction,inhancement of eNOS bioavailability antioxide effect,antiinflammatory properties and reduction of hypertension.Understanding those effects is important for treatment and prevention of cardiovascular disease.

Endothelium-derived hyperpolarizing factor (EDHF) is the third factor released by en-dothelial cell other than NO and PGI2. It relaxes smooth muscle accompanied by a hyperpolarization in the membrane potential. EDHF may be epoxye-icosatrienoic acids (EETs) formed from arachidon-ic acid by the action of cytochrome P450. It is synthesized and/or released by endothelial cell as a result of an cytosolic Ca2+ increase, which is stimulated by the action of acetylcholine or bradykinin on endothelial cell. EDHF is shown to activate Ca2+-activated K+ channels and induce a hyperpolarization in the membrane potential in vascular smooth muscle. The hyperpolarization of the membrane inhibits the opening of voltage-dependentcalcium channels, allows calcium sequestration and removal mechanisms to lower intracellular calcium, and leads smooth muscle to relaxation. In large conducing arteries, EDHF may provide a secondary system to NO, which assumes primary importance in endothelium-dependent relaxation and inhibits the release of EDHF. However, in small resistance arteries, EDHF appears to be a major determinant of vascular calibre, and may be of primary importance in the regulation of vascular resistance.

AIM To investigate the roles of Cl- channels in Ca2+ influx induced by activaion of al- adrenoceptor subtypes in transfected-CHO cells. METHODS The effects of drugs on ?1A、?1B and ?1D- AR-induced Ca2+ influx were investigated with Fura2 fluorescence technique. RESULTS The ?1A-AR- induced Ca2+ influx was inhibited by furosemide(2 .5 ~ 10 M?mol?L- 1 )and SK&F96365(5- 15 ?mol?L- 1 ) in a concentration- dependent manner respectively; The ?1B-AR-induced Ca2+ influx could also be inhibit inhibited by NFA(2. 5 ~ 10 ?mol? L-1 ), whereas the alD AR-induced Ca2+ influx was only suppressed by NFA. In ?1B-CHO cells, Adr-triggered Ca2+ influx could be further inhibited by NFA or furosemide after the maximal inhibition by SK&F96365;SK&F96365 could further inhibit Ca2+ influx which had been inhibited by NFA or furosemide. In ?1A-CHO cells, Adr-triggered Ca2+ influx could be further inhibited by SK&F96365 after had been inhibited by furosemide; furosemide could not further inhibite Ca2+ influx which had been inhibited by S&F96365. CONCLUSION There are different characteristics of CI- channels related to ?1A、 ?1B and ?1D-AR-induced Ca2+ influx.