The effects of artemisin in on the potassium ionic currents of guinea pig ventricular cells and dog Purkinje fibres were studied using the whole cell voltage clamp technique. Artemisin in significantly decreased inward rectifier K+ current (IK1) with an IC50 of (7. 2

Calcium sensing receptors (CaSR) is a member of super-family of G-protein coupling receptors.This review first introduced the concept, construction features, distribution, functions, decision methods, moderators, ge-netic locus of CaSR and its relationship with some diseases concisely. Then this article described the investigation progressof CaSR in cardiovascular system intensively, including the expression pattern, role and signal pathways of CaSR in rat my-ocardium in normal, ischemia-reperfusion injury, apoptosis and cardiac hypertrophy; the role and mechanism of CaSR incalcium homostasis regulation of rat myocardium, endoplasmic reticulum (ER) stress and cardiac ischemic preconditioningand postconditioning. The metabolism rule, physiological significance and pathological action of polyamine in cardiac cells; the increase of CaSR expression in cardiac tissue of artherosclerosic rat and its effect on sensitivity to acute myocardial in-farction are also discussed. In the end, the research perspective of CaSR in cardiovascular system was anticipated.

AIM: To study the effects of berberine on inward rectifier potassium current (Ik1) and outward delayed rectifier potassium current (Ik) of guinea pig ventricular my ocytes, and on human ether-a-go-go related gent (HERG) channel expressed in Xenopus oocytes. METHODS: Whole cell patch-clamp and geneclamp techniques were used to record ionic currents.RESUTS: Berberine prolonged action potential duration (APD) and inhibited Ik1 and Ik in a concentration-dependent manner. Berberine 100μmo1/L increased APD90 from (450±48) ms to (888±90) ms (n=6,P<0.01), and inhibited Ik1 by 64%±7%(n=6,P<0.01). Berberine 50μmo1/L inhibited Ik by 57%±6%,Iktmil by 52%±6%(n=6,P<0.01). Berberine produced a voltage-dependent block on Ik that increased with stronger depolarization, and once all channels activated, there was no further block at positive potentials. Berberine blocked the HERG channels potently with an IC50 value of approximately 75μmo1/L. This block was voltage-dependent, suggesting that it probably bind to either open or inactivated HERG channels. CONCLUSION: Berberine prolonged APD and possessed blocking effect on Ik1,Ik, and HERG channel expressed in Xenopus oocytes. The antiarrhythmic mechanism of berberine is related to its inhibitory effects on Ik1,Ik,and HERG channel.

The expression and function of calcium-sensingreceptor (CaSR) in differentiated THP-1 (human acutemonocytic leukemia cell line) cells are unknown currently.This study investigated above-mentioned issues usingTRAP staining, immunofluorescence staining, Westernblotting, ELISA, and Laser Confocal Scanning Microscopytechniques. We found that CaSR protein was expressed, andmainly located in the membrane and cytoplasm in differentiatedTHP-1 cells. Elevated extracellular calcium orGdCl3 (an agonist of CaSR) raised intracellular calciumconcentration. And this increase was inhibited or abolishedby NPS2390 (an inhibitor of CaSR), U73122 (a specificinhibitor of phospholipase C, PLC) or thapsigargin (a Ca2?-ATPase inhibitor). The extracellular GdCl3 elevation stimulatedboth of IL-1b and TNFa release, and this effect ofGdCl3 was inhibited by NPS2390. In conclusion, CaSR isfunctionally expressed in differentiated THP-1 cells, and theactivated CaSR contributes to intracellular calcium incrementthrough Gq-PLC-inositol triphosphate (IP3) pathwayand commits to cytokine secretion. These results suggestthat CaSR might be involved in a variety of pathologicalprocesses mediated by activated monocyte-macrophages.

n injury by the generation of peroxynitrite. Although polyamines have been implicated in tissue ischemia injury, their metabolism and interactions with NO in myocardial ischemia/reperfusion injury have not been fully understood. In our experiment, when Langendorff perfused rat hearts were subjected to 40 min ischemia without reperfusion, both ornithine decarboxylase (ODC) and Spermidine/spermine N1-acetyltransferase (SSAT) activities were up-regulated and putrescine accumulated. While after reperfusion, ODC activity decreased and SSAT activity increased, resulting in putrescine accumulation and decreased spermidine and spermine. Meanwhile NO content was increased. In addition, sodium nitroprusside (SNP, a NOdonor) decreased ODC activity in cardiac tissue homogenate but increased SSAT activity in a dose-dependent manner. Pre-treatment of isolated heart with Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME, an inhibitor of NO synthase) increased ODC activity. Exogenous spermine (1 mM) administration prior to ischemia prevented spermine decrease, reduced cardiac myocyte necrosis and apoptosis, and promoted the recovery of cardiac function after ischemia/reperfusion. These results suggest that acute heart ischemia activates myocardial polyamine stress response characterized by increased ODC and SSAT activities and accumulation of putrescine. Ischemia/reperfusion disturbs polyamine metabolism, and the loss of spermine might be associated with NO increase and thereby influences myocardial cell viability. Exogenous spermine may protect the hearts from myocardial ischemia/reperfusion injury.