Direct gastrin action on isolated rat parietal cells induces morphological transformations

Area of Science:

• Cell Biology
• Gastroenterology
• Physiology

Background:

• Gastrin's potentiating effect on histamine and dibutyryl-cAMP (DBcAMP) stimulated aminopyrine accumulation in rat parietal cells was previously reported.
• The precise mechanism of gastrin's action on parietal cells requires further investigation.

Purpose of the Study:

• To investigate the mechanism by which gastrin potentiates the stimulatory action of histamine and DBcAMP on parietal cells.
• To determine if gastrin directly influences parietal cell morphology and metabolic activity.

Main Methods:

• Isolated rat parietal cells were incubated under various conditions.
• Morphometric analysis of electron micrographs was performed to assess vacuolar/canalicular spaces.
• Aminopyrine accumulation and [14C]glucose oxidation were measured to evaluate cell activity.
• Histamine H2-receptor antagonist ranitidine was used to differentiate receptor-mediated effects.

Main Results:

• Pentagastrin induced vacuolar/canalicular spaces similar to histamine, an effect not blocked by ranitidine.
• Combined pentagastrin and histamine stimulation resulted in a 2-fold increase in vacuolar/canalicular volume.
• Gastrin-17 (G-17) potentiated histamine-stimulated aminopyrine accumulation, an effect blocked by ranitidine.
• G-17 also potentiated DBcAMP stimulation, independent of ranitidine.
• Pentagastrin increased basal glucose oxidation, unaffected by ranitidine, while histamine's effect was blocked.

Conclusions:

• Gastrin directly acts on parietal cells to potentiate histamine's effect on aminopyrine accumulation by increasing vacuolar/canalicular spaces.
• Gastrin's primary role appears to be inducing a stimulated cell morphology rather than direct ion transport activation.
• These morphological changes are reflected in the metabolic activity of the parietal cells.