Lee K Y, Biancani P, Behar J
Department of Medicine, Rhode Island Hospital, Providence 02902.
Am J Physiol. 1989 Apr;256(4 Pt 1):G785-8. doi: 10.1152/ajpgi.1989.256.4.G785.
The calcium sources responsible for gallbladder contraction in response to cholecystokinin (CCK) and acetylcholine were studied in vitro in the cat. Sudden replacement of normal physiological salt solution (PSS) with calcium-free PSS blocked the contraction induced by KCl (60 mM) but did not affect the response to CCK (10(-7) M) or acetylcholine (3 x 10(-3) M). Thirty-minute incubation in PSS in which strontium (2.5 mM) was substituted for calcium blocked completely CCK (10(-10) - 10(-6) M)-induced contraction without impairing the response to acetylcholine (10(-7) - 10(-3) M) or KCl (20-80 mM). The contraction induced by acetylcholine (10(-7) - 10(-3) M) was partially blocked by hydroxyverapamil (D-600) (10(-5) M) in normal PSS (Ca 2.5 mm) and was completely blocked by D-600 in strontium (2.5 mm)-containing solution. It is concluded that CCK contracts the gallbladder muscle by mobilizing calcium from intracellular stores, whereas acetylcholine can utilize calcium both from intracellular or extracellular sources.