Properties of the contraction produced by PGF2 alpha in the guinea-pig taenia coli were compared to those produced by ACh. Prostaglandin (PG) F2 alpha (3 x 10(-7) M) and acetylcholine (ACh, 10(-5)M) induced an initial transient contraction (phasic contraction) and a subsequent late contraction (tonic contraction). Both phasic and tonic contractions produced by PGF2 alpha or ACh were abolished in Ca2+ -free Krebs solution containing 0.5 mM EGTA. The tonic contractions caused by PGF2 alpha and ACh were markedly suppressed by alpha-[3-[[2-(3,4-dimethoxy-phenyl)-ethyl]-methylamino]-propyl]- 3,4,5-trimethoxy-alpha-(1-methylethyl)benzeneacetonitrile hydrochloride (D600, greater than 10(-7)M) as well as nifedipine (5 x 10(-9)M), a Ca2+-antagonist. However, the phasic contraction produced by PGF2 alpha, but not by ACh, was greatly inhibited by Mn2+ (greater than 10(-4)M). Furthermore, the phasic contraction caused by PGF2 alpha was abolished in 18 mM K+ Krebs solution with D600 (2 x 10(-7)M), whereas that induced by ACh and the tonic contractions produced by PGF2 alpha as well as by ACh were unaffected in this high K+ solution without D600. Membrane potentials of the tissue in normal (K+, 5.9 mM) and 18 mM K+ Krebs solution containing D600 were about -55 mV and -43 mV, respectively. In a fluorescence study which used Fura-2 an intracellular free Ca2+ indicator in the presence of D600, PGF2 alpha and ACh increased fluorescence intensity in the tissue, which coupled with the magnitude of contractions.(ABSTRACT TRUNCATED AT 250 WORDS)