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Acute but not chronic gastric sodium administration regulates vasoactive intestinal peptide metabolism by the liver
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We have shown previously that gastric sodium loading releases vasoactive intestinal peptide from the intestine and in rabbits on a low sodium diet it appears to decrease vasoactive intestinal peptide metabolism by the liver. To determine the contributions of the low sodium diet and the acute sodium load to changes in vasoactive intestinal peptide metabolism, metabolic clearance studies of vasoactive intestinal peptide infused intraportally were performed. These studies were performed in male New Zealand white rabbits equilibrated on normal and low sodium diets before and after an acute gastric sodium load of 1.5 mmol kg‐1. No difference was detectable in metabolic clearance rates between normal and low salt diets, however, decreases in metabolic clearance rates were observed in response to the sodium load (normal diet P < 0.005, low salt P < 0.0005). Secretion rates also decreased following the gastric sodium load (normal P < 0.005, low salt P < 0.05).We conclude that hepatic VIP metabolism is decreased by acute gastric sodium loading but it is not affected by chronic sodium intake.
Title: Acute but not chronic gastric sodium administration regulates vasoactive intestinal peptide metabolism by the liver
Description:
We have shown previously that gastric sodium loading releases vasoactive intestinal peptide from the intestine and in rabbits on a low sodium diet it appears to decrease vasoactive intestinal peptide metabolism by the liver.
To determine the contributions of the low sodium diet and the acute sodium load to changes in vasoactive intestinal peptide metabolism, metabolic clearance studies of vasoactive intestinal peptide infused intraportally were performed.
These studies were performed in male New Zealand white rabbits equilibrated on normal and low sodium diets before and after an acute gastric sodium load of 1.
5 mmol kg‐1.
No difference was detectable in metabolic clearance rates between normal and low salt diets, however, decreases in metabolic clearance rates were observed in response to the sodium load (normal diet P < 0.
005, low salt P < 0.
0005).
Secretion rates also decreased following the gastric sodium load (normal P < 0.
005, low salt P < 0.
05).
We conclude that hepatic VIP metabolism is decreased by acute gastric sodium loading but it is not affected by chronic sodium intake.
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