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1 Department of Surgery, Stanford University, Stanford 94305; and 2 Departments of Medicine and Physiology, Cardiovascular Research Institute, University of California, San Francisco, California 94143-0521
The
aquaporin-4 (AQP4) water channel has been proposed to play a role in
gastric acid secretion. Immunocytochemistry using anti-AQP4
antibodies showed strong AQP4 protein expression at the basolateral
membrane of gastric parietal cells in wild-type (+/+) mice. AQP4
involvement in gastric acid secretion was studied using transgenic null
(
/) mice deficient in AQP4 protein. / Mice had grossly normal
growth and appearance and showed no differences in gastric morphology
by light microscopy. Gastric acid secretion was measured in
anesthetized mice in which the stomach was luminally perfused (0.3 ml/min) with 0.9% NaCl containing [14C]polyethylene
glycol ([14C]PEG) as a volume marker. Collected effluent
was assayed for titratable acid content and [14C]PEG
radioactivity. After 45-min baseline perfusion, acid secretion was
stimulated by pentagastrin (200 µg · kg
1
· h1 iv) for 1 h or histamine (0.23 mg/kg iv) + intraluminal carbachol (20 mg/l). Baseline gastric acid secretion
(means ± SE, n = 25) was 0.06 ± 0.03 and
0.03 ± 0.02 µeq/15 min in +/+ and / mice, respectively.
Pentagastrin-stimulated acid secretion was 0.59 ± 0.14 and
0.70 ± 0.15 µeq/15 min in +/+ and / mice, respectively. Histamine plus carbachol-stimulated acid secretion was 7.0 ± 1.9 and 8.0 ± 1.8 µeq/15 min in +/+ and / mice, respectively.
In addition, AQP4 deletion did not affect gastric fluid secretion, gastric pH, or fasting serum gastrin concentrations. These results provide direct evidence against a role of AQP4 in gastric acid secretion.
water transport; stomach; gastrin; transgenic mice
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