To explain that bronchial smooth muscle undergoes sustained agonist-induced contractions in a Ca(2+)-free medium, we hypothesized that caveolae in the plasma membrane (PM) contain protected Ca(2+). We isolated caveolae from canine tracheal smooth muscle by detergent treatment of PM-derived microsomes. Detergent-resistant membranes were enriched in caveolin-1, a specific marker for caveolae as well as for L-type Ca(2+) channels and Ca(2+) binding proteins (calsequestrin and calreticulin) as determined by Western blotting. Also, the PM Ca(2+) pump was present but not connexin 43 (a noncaveolae PM protein), the sarcoplasmic reticulum (SR) Ca(2+) pump, or the type 1 inositol 1,4, 5-trisphosphate receptor, supporting the idea that SR-derived membranes were not present. Antibodies to caveolin coimmunoprecipitated caveolin with calsequestrin or calreticulin. Thus some of the cellular calsequestrin and calreticulin associated with caveolin on the cytoplasmic face of each caveola. Immunohistochemistry of tracheal smooth muscle crysosections confirmed the localization of caveolin and the PM Ca(2+) pump to the cell periphery, whereas the SR Ca(2+) pump was located deeper in the cell. The presence of L-type Ca(2+) channels, the PM Ca(2+) pump, and the Ca(2+) bindng proteins calsequestrin and calreticulin in caveolin-enriched membranes supports caveola involvement in airway smooth muscle Ca(2+) handling.

The store-operated Ca2+ entry (SOCE) pathway has aroused much interest recently not only because of its unusual nature as retrograde signaling, but also due to its wide occurrence and its possible role in physiological and pathophysiological situations. A number of synthetic or naturally occurring drugs recently used to block this Ca2+ entry pathway are briefly reviewed. Although important and interesting information has been obtained using these putative SOCE blockers described in this review, they indeed have sites of action other than the SOCE channels, and caution must be exercised in using them as putative tools to study SOCE. For instance, the highly variable potency of some synthetic blockers (SK&F 96365 and LOE 908) to inhibit SOCE has provided indirect evidence for the heterogeneous nature of the SOCE channels, an observation consistent with the differential Mn2+ permeability through SOCE in various cell types. The use of SK&F 96365 at relatively high concentrations has unexpectedly revealed its potential as an opener of a novel cation entry pathway. The ability of LU52396 to discriminate the SOCE channel in its closed/open states may be useful in the analysis of the kinetics of SOCE channel activation/inactivation. The possible presence of both agonistic and antagonistic saponins derived from ginseng plants for the study of SOCE deserves more rigorous experimental investigations, which may lay new ground for the development of new types of Ca2+ antagonists (and/or agonists) from the natural resources.

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The addition of Ca2+ ionophore A23187 or ATP to freshly isolated or cultured pig coronary artery endothelial cells (PCEC) potentiated the release of ascorbate (Asc). Cultured PCEC were used to characterize the Ca2+‐mediated release. An increase in Ca2+‐mediated Asc release was observed from PCEC preincubated with Asc, Asc‐2‐phosphate or dehydroascorbic acid (DHAA). The effects of various ATP analogs and inhibition by suramin were consistent with the ATP‐induced release being mediated by P2Y2‐like receptors. ATP‐stimulated Asc release was Ca2+‐mediated because (a) ATP analogs that increased Asc release also elevated cytosolic [Ca2+], (b) Ca2+ ionophore A23187 and cyclopiazonic acid stimulated the Asc release, (c) removing extracellular Ca2+ and chelating intracellular Ca2+inhibited the ATP‐induced release, and (d) inositol‐selective phospholipase C inhibitor U73122 also inhibited this release. Accumulation of Asc by PCEC was examined at Asc concentrations of 10 μM (Na+‐Asc symporter not saturated) and 5 mM (Na+‐Asc symporter saturated). At 10 μM Asc, A23187 and ATP caused an inhibition of Asc accumulation but at 5 mM Asc, both the agents caused a stimulation. Substituting gluconate for chloride did not affect the basal Asc uptake but it abolished the effects of A23187. PCEC but not pig coronary artery smooth muscle cells show a Ca2+‐ mediated Asc release pathway that may be activated by agents such as ATP. British Journal of Pharmacology (2006) 147, 131–139. doi:

This paper presents a comprehensive statistical report on China’s current apparel retailing environment, including the macro‐ (demographic, economic, political, cultural, technological and natural factors) and micro‐ (sourcing, garment manufacturing, marketing intermediaries and consumers) environments affecting foreign investments in China’s apparel retailing market. With an examination of China’s demographic and economic indicators over the past 20 years, and the changing pattern of other macro‐factors having typically influenced the foreign investments in China’s apparel retailing sector, the paper also investigates the prevailing micro‐factors facing foreign investors. The future prospects of the China apparel retailing industry were also discussed.