Four dogs with chronic gastric
fistulas were give intravenous
bombesin nonapeptide (B9),
ranatensin, and
litorin by constant infusion for 90 min at 1.2 micrograms x kg-1 on separate days. A dose response study with
substance P (1.5, 3.0, 60, 18 and 54 micrograms x kg-1 x h-1) was also carried out and all tests compared to a standard
protein meal (10g x kg-1). Plasma
gastrin and PP were measured by radioimmunoassay and gastric acid by autobiuret titration.
Substance P failed to stimulate gastric acid secretion or release either
pancreatic polypeptide (PP) or
gastrin. Basal
gastrin levels were 8 +/-2 fmol/ml. The peak increment of
gastrin released by
bombesin was 95 +/- 16,
ranatensin 22 +/- 6,
litorin 18 +/- 4, and meal 39 +/- 5 fmol/ml.
Bombesin caused significantly greater release of
gastrin than a meal,
litorin or
ranatensin (P less than 0.01). Basal gastric secretion was 23 +/- 4 microequiv./min. B9 produced a peak
acid secretion of 356 +/- 124 muequiv./min. There was no significant difference between the
bombesin-like
peptides (P less than 0.01). Basal plasma PP was 38 +/- 12 fmol/ml. B9 produced a peak PP increment of 600 +/- 50,
litorin 137 +/- 36,
ranatensin 98 +/- 11, and a meal 305 +/- 58 fmol/ml. B9 released significantly more PP than either
litorin of
ranatensin (P less than 0.01). The different amino acid sequences of the
peptides are probably responsible for their potency. The substitution of a penultimate
phenylalanine residue in
litorin and
ranatensin for
leucine in
bombesin does not prevent PP or
gastrin release by
bombesin-like
peptides. Since
bombesin-like
peptides are widely distributed in the gastrointestinal tract of man and stimulate both
acid and gut
hormone secretion, it is possible that they might play a physiological role in the modulation of gastrointestinal function.