Search

Your search keyword '"Du, Xiao-yi"' showing total 29 results
Start Over Author "Du, Xiao-yi"
29 results on '"Du, Xiao-yi"'

14. Cardiac swelling-induced chloride current depolarizes canine atrial myocytes

Author

Du, Xiao-Yi and Sorota, Steve

Subjects
Heart cells -- Physiological aspects, Action potentials (Electrophysiology) -- Research, Chlorides in the body -- Physiological aspects, Heart ventricles -- Physiological aspects, Biological sciences
Abstract

The depolarized dog atrial myocytes were analyzed to determine the effects of swelling-induced chloride currents (ICl,swell) on the transmembrane resting potential. The depolarization of dog atrial myocytes led to the activation of ICl,swell which was inhibited by the administration of niflumic acid. The reversal potential for ICl,swell was also shifted by the substitution of extracellular chloride with SCN- ions. Furthermore, the resting membrane was depolarized by the activation of ICl,swell in canine atrial cells.

Published
1997

19. Mild moxibustion at different intervention times on the levels of ET-1 and NO in the uterine tissues of rats with cold-damp coagulation and stagnation type dysmenorrhea

Author

SUN, Xiao-xue, YANG, Li-yun, LIANG, Yu-lei, LI, Xin-hua, GAO, Fei, DU, Xiao-yi, ZHOU, Xiao-hong, CHEN, Yang, LI, Xue-na, and SUN, Li-hong

Abstract

To observe the differences in analgesic effect of moxibustion at different intervention times on dysmenorrhea rats and explore its effect mechanism.

Published
2024
Full Text
View/download PDF

28. Isoprenaline can activate the acetylcholine‐induced K+current in canine atrial myocytes via Gs‐derived βγ subunits

Author

Sorota, Steve, Rybina, Irina, Yamamoto, Ai, and Du, Xiao‐Yi

Abstract

1G protein βγ subunits activate the acetylcholine‐induced potassium current Ik,ach. There is no evidence of specificity at the level of the βγ subunits. Therefore all G protein‐coupled receptors in atrial myocytes should be able to activate Ik,ach. Paradoxically, it is often stated that isoprenaline does not activate Ik,ach. Rationales to explain this negative result include insufficient concentrations of Gsin the atrium or restricted access of Gs‐derived βγ subunits to the Ik,achchannel. We took advantage of a non‐specific increase in Gsthat results after infection with adenovirus.2Adenoviral infection unmasked a 1 μmisoprenaline‐induced Ik,achwhich was prevented by propranolol. Isoprenaline occasionally activated Ik,achin uninfected and freshly dissociated atrial myocytes but the effect was larger and more consistent in infected myocytes.3Pertussis toxin pretreatment (100 ng ml−1overnight) did not block the effect of isoprenaline. The effect of isoprenaline became persistent if cells were pretreated with cholera toxin (200 ng nl−1).4Signal transduction events distal to adenylyl cyclase were not involved in isoprenaline‐induced Ik,ach. Forskolin (10 μm) did not activate Ik,ach. Inhibition of adenylyl cyclase with cytoplasmic application of 300 μm2′‐deoxyadenosine 3′‐monophosphate did not prevent the activation of Ik,achby isoprenaline.5Cytoplasmic application of a βγ binding peptide derived from the C terminus of β‐adrenergic receptor kinase 1 (50 μm) prevented the effect of isoprenaline on Ik,ach. The peptide did not prevent the stimulation of the L‐type calcium current by isoprenaline.6The results indicate that β‐adrenoceptors can activate Ik,achin atrial myocytes through the release of βγ subunits from Gs.

Published
1999
Full Text
View/download PDF

29. Structural determinants for histamine H1 affinity, hERG affinity and QTc prolongation in a series of terfenadine analogs

Author

Aslanian, Robert, Piwinski, John J., Zhu, Xiaohong, Priestley, Tony, Sorota, Steve, Du, Xiao-Yi, Zhang, Xue-Song, McLeod, Robbie L., West, Robert E., Williams, Shirley M., and Hey, John A.

Subjects
*STRUCTURAL analysis (Science), *HISTAMINE, *TERFENADINE, *ANTIHISTAMINES, *ASTEMIZOLE, *TACHYARRHYTHMIAS, *VENTRICULAR fibrillation
Abstract

Abstract: In the late 1980’s reports linking the non-sedating antihistamines terfenadine and astemizole with torsades de pointes, a form of ventricular tachyarrhythmia that can degenerate into ventricular fibrillation and sudden death, appeared in the clinical literature. A substantial body of evidence demonstrates that the arrhythmogenic effect of these cardiotoxic antihistamines, as well as a number of structurally related compounds, results from prolongation of the QT interval due to suppression of specific delayed rectifier ventricular K+ currents via blockade of the hERG-IKr channel. In order to better understand the structural requirements for hERG and H1 binding for terfenadine, a series of analogs of terfenadine has been prepared and studied in both in vitro and in vivo hERG and H1 assays. [Copyright &y& Elsevier]

Published
2009
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results