In-Vitro effect of Ficus deltoidea on the contraction of isolated rat’s uteri is mediated via multiple receptors binding and is dependent on extracellular calcium

Article

Author: Naguib Salleh ; Vivi Noryati Ahmad

BACKGROUNDFicus deltoidea, is a perennial herb that is used to assist labor, firm the uterus post-delivery and to prevent postpartum bleeding. In view of its claimed uterotonic action, the mechanisms underlying plant's effect on uterine contraction were investigated.METHODSAdult female SD rats were injected with 2 mg/kg 17β-oestradiol (E2) to synchronize their oestrous cycle. A day after injection, uteri were removed for in-vitro contraction studies. The dose dependent effect of Ficus deltoidea aqeous extract (FDA) on the tension produced by the isolated rat's uteri was determined. The effects of atropine (2×10(-8) M), atosiban (0.5 IU), THG113.31 (10 μM), oxodipine (0.25 mM), EDTA (1 mM), 2-amino-ethoxy-diphenylborate (2-APB) (40 mM) and thapsigargin (1 mM) on the maximum force of contraction (Emax) achieved following 2 mg/ml FDA administration were also investigated.RESULTSFDA induced in-vitro contraction of the isolated rat's uteri in a dose-dependent manner. Administration of atropine, atosiban and THG113.31 reduced the Emax with atosiban having the greatest effect. The Emax was also reduced following oxodipine and EDTA administration. There was no significant change observed following 2-APB administration. Thapsigargin, however, augmented Emax.CONCLUSIONSFDA-induced contraction of the isolated rat's uteri is mediated via multiple uterotonin receptors (muscarinic, oxytocin and prostaglandin F2α) and was dependent on the extracellular Ca2+. Contraction, however, was not dependent on the Ca2+ release from the internal stores. This in-vitro study provides the first scientific evidence on the claimed effect of Ficus Deltoidea on uterine contraction.

01 Jun 2003·The Journal of PhysiologyQ2 · MEDICINE

Stimulation of L‐type Ca²⁺ Channels by Inositol Pentakis‐ and Hexakisphosphates in Rat Vascular Smooth Muscle Cells

Q2 · MEDICINE

Article

Author: Mironneau, C. ; Quignard, J. F. ; Rakotoarisoa, L. ; Mironneau, J.

The electrophysiological effects of d‐myo‐inositol 1,3,4,5,6‐pentakisphosphate (InsP5) and d‐myo‐inositol hexakisphosphate (InsP6), which represent the main cellular inositol polyphosphates, were studied on L‐type Ca2+ channels in single myocytes of rat portal vein. Intracellular infusion of InsP5 (up to 50 μm) or 10 μm InsP6 had no action on Ba2+ current, whereas 50 μm InsP6 or 10 μm InsP5 plus 10 μm InsP6 (InsP5,6) stimulated the inward current. The stimulatory effect of InsP5,6 was also obtained in external Ca2+‐containing solution. The stimulated Ba2+ current retained the properties of L‐type Ba2+ current and was oxodipine sensitive. PKC inhibitors Ro 32‐0432 (up to 500 nm), GF109203X (5 μm) or calphostin C (100 nm) abolished the InsP5,6‐induced stimulation. Neither the PKA inhibitor H89 (1 μm) nor the protein phosphatase inhibitors okadaic acid (500 nm) or cypermethrin (1 μm) prevented or mimicked the InsP5,6‐induced stimulation of Ba2+ current. However, InsP5 or InsP6 could mimic some effects of protein phosphatase inhibitor so as to extend after washing‐out forskolin the stimulatory effects of the adenylyl cyclase activator on Ba2+ current. These results indicate that InsP5 and InsP6 may act as intracellular messengers in modulating L‐type Ca2+ channel activity and so could be implicated in mediator‐induced contractions of vascular smooth muscle cells.

01 Jul 1999·American Journal of Physiology-Cell Physiology

Norepinephrine-induced Ca²⁺waves depend on InsP₃ and ryanodine receptor activation in vascular myocytes

Article

Author: Boittin, François-Xavier ; Mironneau, Jean ; Halet, Guillaume ; Macrez, Nathalie

In rat portal vein myocytes, Ca2+ signals can be generated by inositol 1,4,5-trisphosphate (InsP3)- and ryanodine-sensitive Ca2+ release channels, which are located on the same intracellular store. Using a laser scanning confocal microscope associated with the patch-clamp technique, we showed that propagated Ca2+ waves evoked by norepinephrine (in the continuous presence of oxodipine) were completely blocked after internal application of an anti-InsP3 receptor antibody. These propagated Ca2+ waves were also reduced by ∼50% and transformed in homogenous Ca2+ responses after application of an anti-ryanodine receptor antibody or ryanodine. All-or-none Ca2+ waves obtained with increasing concentrations of norepinephrine were transformed in a dose-response relationship with a Hill coefficient close to unity after ryanodine receptor inhibition. Similar effects of the ryanodine receptor inhibition were observed on the norepinephrine- and ACh-induced Ca2+ responses in non-voltage-clamped portal vein and duodenal myocytes and on the norepinephrine-induced contraction. Taken together, these results show that ryanodine-sensitive Ca2+release channels are responsible for the fast propagation of Ca2+ responses evoked by various neurotransmitters producing InsP3in vascular and visceral myocytes.

100 Deals associated with Oxodipine

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Indication	Highest Phase	Country/Location	Organization	Date
Hypertension	Phase 3	ES	Iqb	-
Hypertension	Phase 3	FR	-	-
Hypertension	Phase 3	DE	-	-

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