The effect of calcitonin on meal-stimulated gallbladder emptying (GBE) was examined after intravenous (i.v.) and intracerebroventricular (i.c.v.) administration in six mongrel dogs. The gallbladder contraction was surveyed by means of real-time ultrasonography in conscious dogs. Calcitonin given i.v. elicited an immediate and strong inhibition of postprandial GBE-the integrated 0- to 120-min gallbladder response was 118.1 +/- 8.0%.h after placebo, whereas it was 91.8 +/- 2.1%.h, 59.4 +/- 17.9%.h (P < 0.001), and 14.2 +/- 20.5%.h (P < 0.001) after 3.6, 18.0, and 90.0 pmol.kg-1 calcitonin, respectively. After i.c.v. administration (1.8 and 18.0 pmol.kg-1), only the higher calcitonin dose exerted a moderate inhibitory effect on postprandial GBE. The calcitonin doses required to evoke a 50% inhibition of meal-stimulated GBE were 15- to 10-fold lower after i.v. than i.c.v. application. Peripherally given calcitonin brought about a dose-dependent increase in the interdigestive gallbladder volume-the linear regression of the relative gallbladder volume versus calcitonin dose was y = 11.60 [ln(dose + 1)] + 97.02 (r = 0.864, P < 0.001). Intravenous application of calcitonin did not affect caerulein-induced GBE. The results obtained imply that: (i) calcitonin exerts an inhibitory influence on meal-induced GBE and that this effect is more pronounced after i.v. than after i.c.v. administration, and (ii) peripherally given calcitonin does not inhibit caerulein-induced gallbladder contraction in the dog.
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Department of Physiology, Graduate School of Medical and Dental Sciences, Kagoshima University, Sakuragaoka 8-35-1, 890-8544, Kagoshima, Japan. Electronic address:
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