The Role of Sodium in Somatostatin Secretion: Evidence for the Involvement of Na+Channels in the Release Mechanism*

Publisher Website
Google Scholar
Abstract
The influence of Na+ upon the secretion of somatostatin from the isolated perfused canine pancreas was studied. The Na+ channel-opening alkaloid veratridine (10 μm) was found to cause a biphasic increase in somatostatin output at a normal Ca++ concentration of 1.3 nm. The response to veratridine was inhibited 70% by the addition of 1 μm tetrodotoxin (TTX) and was totally abolished in the absence of extracellular Ca++. TTX (1 μm) reversibly inhibited (by 30%) the glucoseinduced somatostatin secretion. During Ca++ depletion, the inhibitory effect of TTX was eliminated. Partial replacement of extracellular Na+ by choline (40 DIM Na+ and 100 mm choline) caused a 3- to 4-fold increase in somatostatin secretion. This finding and the fact that the somatostatin response to Na+ withdrawal required the presence of extracellular Ca++ suggest that the stimulatory effect of a decrease in extracellular Na+ concentration is mediated, at least in part, by a Na+-Ca++ countertransport mechanism. The results indicate that the Na+-mediated somatostatin release is dependent upon the extracellular Ca++ concentration. It is unlikely that Na+ per se or via redistribution of the intracellularly bound Ca++ can stimulate somatostatin secretion. (Endocrinology106: 1843, 1980)

This publication has 2 references indexed in Scilit: