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The periodic spike-burst response of pancreatic beta-cells varies in duration with an increase of external glucose within the range 5-20 mM. To elucidate the mechanism determining the length of spike-burst, we studied the low-Na+ induced change in electrical response to glucose which is similar to the change induced by high glucose. Cytoplasmic pH (pHi) and Ca2+ concentration ([Ca2+]i) were measured by the microfluorometric method under normal and low-Na+ conditions in mouse pancreatic islets. Lowering external Na+ concentration from 135 to 25 mM by replacing Na+ with Tris+ induced progressive alkalinization in islet cells in the presence of 11.1 mM glucose. In contrast, reduction of external Na+ by replacement with Li+ caused intracellular acidification. Both manipulations described above caused a marked increase in [Ca2+]i, suggesting the presence of Na+/Ca(2+)-antiport activity. Although the change in pHi induced by decreasing external Na+ varied in direction depending on the species of cations used for replacing Na+, the pattern of electrical activity consistently changed from the spike-burst type to the continuous spike-generation type without regard for the difference in species of cations replacing Na+. These findings lead to the following hypothesis: A decrease in Na+ influx could cause a decrease in ATP-consumption by Na+/K(+)-pumps that prevents the fall of intracellular ATP concentration. The resultant continuation of high concentrations of intracellular ATP may be responsible for the abolishment of the silent phase.

We evaluated the activation and destruction of platelets in 24 patients with rheumatic heart disease (RHD) involving the mitral valve. Ex vivo platelet aggregation induced by adenosine diphosphate (ADP) and collagen was significantly increased in RHD patients as compared with normal controls. Plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 were also elevated. Plasma concentrations of glycocalicin, a proteolytic fragment of platelet membrane glycoprotein Ib, were increased, while platelet counts were decreased in RHD patients as compared with normal controls. RHD patients with, versus those without, atrial fibrillation demonstrated significant differences in beta-TG levels and platelet counts. However, we observed no difference in glycocalicin levels between the two groups. The present study demonstrated that increased platelet activation, as well as platelet destruction, occur in patients with RHD.

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