Resveratrol and genistein inhibition of rat isolated gastrointestinal contractions and related mechanisms.

AIM: To investigate the effects and underlying mechanisms of resveratrol and genistein on contractile responses of rat gastrointestinal smooth muscle. METHODS: Isolated strips of gastrointestinal smooth muscle from Spraque-Dawley rats were suspended in organ baths containing Kreb's solution, and the contractility of smooth muscles was measured before and after incubation with resveratrol and genistein, and the related mechanisms were studied by co-incubation with various inhibitors. RESULTS: Resveratrol and genistein dose-dependently decreased the resting tension, and also reduced the mean contractile amplitude of gastrointestinal smooth muscle. Estrogen receptor blockades (ICI 182780 and tamoxifen) failed to alter the inhibitory effects induced by resveratrol and genistein. However, their effects were attenuated by inhibitions of α-adrenergic receptor (phentolamine), nitric oxide synthase (levorotatory-NG-nitroarginine), ATP-sensitive potassium channels (glibenclamide), and cyclic adenosine monophosphate (SQ22536). In high K(+)/Ca(2+)-free Kreb's solution containing 0.01 mmol/L egtazic acid, resveratrol and genistein reduced the contractile responses of CaCl2, and shifted its cumulative concentration-response curves rightward. CONCLUSION: Resveratrol and genistein relax gastrointestinal smooth muscle via α-adrenergic receptors, nitric oxide and cyclic adenosine monophosphate pathways, ATP-sensitive potassium channels, and inhibition of L-type Ca(2+) channels.

[Inhibitory effects of 17beta-estradiol on spontaneous and activated contraction of rat uterus smooth muscle].

OBJECTIVE: To observe and compare the effects of 17beta-estradiol (EST) on the phasic and tonic contractile activities of the uterine smooth muscles of SD rats in vitro. METHODS: Different concentrations of 17beta-estradiol were added into the perfusion muscular sockets containing uterine smooth muscles of SD rats, and the activities of muscle contraction were recorded at the same time. RESULTS: 17beta-estradiol had obvious depression effects on spontaneous rhythmic contraction of the uterine smooth muscles in a concentration-dependent manner, it could considerably decrease muscular tension, the mean amplitudes and frequencies of contractile waves (P < 0.01); it could also suppress the uterine contraction stimulated by KCl, CaCl2 or prostaglandin F2alpha (PGF2alpha). Based on the contraction of uterine smooth muscle stimulated by KCl, IC50 was 7.278 micromol/L and pD2 was -0.862 when calculated by linear regression method. 17beta-estradiol could also inhibit the maximal CaC12 contraction of uterine smooth muscle in the Ca2+ free Krebs solution, which the ECQ was 1.422 x 10(-3) mol/L, pD2 was 2.847 (control), but the E50 was 3.028 x 10(-3) mol/L, p2 was 2.519 (added with EST) when calculated by linear regression method. CONCLUSION: The depression effects of 17beta-estradiol on the spontaneous rhythmic contraction and activated contraction of the uterine smooth muscles of SD rats could be mediated through the blockage of C2+ influx through potential-dependent Ca2+ channels of plasma membrane.