Abstract
The simple model shown in Fig. 1 can be used to explain pancreatic acinar stimulus-secretion coupling by assuming that the Ca-activated cation channel is not perfectly selective for mono-valent cations, but enables a very slight leak of divalent cations. Stimulation by ACh or CCK releases intracellular Ca (probably from the plasma membrane) raising [Ca++]i. This opens up the 30-35 pS channels giving rise to Na influx and depolarization. At the same time Ca can leak into the cells through the same channels, maintaining an elevated [Ca++]i. Removal of agonist (and/or inclusion of antagonist) causes a rapid reuptake of Ca into the trigger pool (Stolze and Schulz 1980) causing a decrease in [Ca++]i and closure of the channel with rapid return to the resting potential and the resting [Ca++]i.
| Original language | English |
|---|---|
| Pages (from-to) | 82-84 |
| Number of pages | 3 |
| Journal | Pflügers Archiv European Journal of Physiology |
| Volume | 396 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 1983 Jan 1 |
ASJC Scopus subject areas
- Physiology
- Clinical Biochemistry
- Physiology (medical)