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Research Article

In vitro determination of the mechanism of the uterine stimulatory effect of Newbouldia laevis

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Pages 808-815 | Received 12 Mar 2009, Accepted 23 Jun 2009, Published online: 30 Apr 2010

Figures & data

Table 1. Effect of antagonists on the EC50 of EEN.

Table 2. Effect of antagonists on the EC50 of oxytocin.

Figure 1. Concentration-response curves showing the uterine contractile response of the ethanol extract of N. laevis (EEN) in the absence and presence of phentolamine (PHEN). There was no significant difference in the Emax of EEN (n = 6 rats).

Figure 1.  Concentration-response curves showing the uterine contractile response of the ethanol extract of N. laevis (EEN) in the absence and presence of phentolamine (PHEN). There was no significant difference in the Emax of EEN (n = 6 rats).

Figure 2. Concentration-response curves showing the contractile response of oxytocin in the presence and absence of phentolamine (PHEN). There was no significant difference in the Emax of oxytocin (n = 6 rats).

Figure 2.  Concentration-response curves showing the contractile response of oxytocin in the presence and absence of phentolamine (PHEN). There was no significant difference in the Emax of oxytocin (n = 6 rats).

Figure 3. Concentration-response curves of the effect of diphenhydramine (DPH) on the ethanol extract of N. laevis. DPH inhibited the effect of the extract but there was no significant difference in the Emax of EEN (n = 6 rats).

Figure 3.  Concentration-response curves of the effect of diphenhydramine (DPH) on the ethanol extract of N. laevis. DPH inhibited the effect of the extract but there was no significant difference in the Emax of EEN (n = 6 rats).

Figure 4. Concentration-response curves of the effect of diphenhydramine (DPH) on oxytocin-induced uterine contraction. No inhibition was observed and there was no significant difference in the Emax of oxytocin (n = 6 rats).

Figure 4.  Concentration-response curves of the effect of diphenhydramine (DPH) on oxytocin-induced uterine contraction. No inhibition was observed and there was no significant difference in the Emax of oxytocin (n = 6 rats).

Figure 5. Concentration-response curves showing uterine response to EEN in the presence and absence of atropine (ATR). ATR inhibited the effect of the extract but there was no significant difference in the Emax (n = 6 rats).

Figure 5.  Concentration-response curves showing uterine response to EEN in the presence and absence of atropine (ATR). ATR inhibited the effect of the extract but there was no significant difference in the Emax (n = 6 rats).

Figure 6. Concentration-response curves of oxytocin-induced uterine contraction in the presence of atropine (ATR). No inhibition was observed (n = 6 rats).

Figure 6.  Concentration-response curves of oxytocin-induced uterine contraction in the presence of atropine (ATR). No inhibition was observed (n = 6 rats).

Figure 7. Concentration-response curves of EEN in the presence of verapamil (VER). VER shifted the curve to the right and significantly depressed (p <0.01) the Emax (n = 6 rats).

Figure 7.  Concentration-response curves of EEN in the presence of verapamil (VER). VER shifted the curve to the right and significantly depressed (p <0.01) the Emax (n = 6 rats).

Figure 8. Concentration-response curves of oxytocin alone and in the presence of verapamil (VER). VER significantly depressed (p <0.01) the Emax and shifted the curve to the right (n = 6 rats).

Figure 8.  Concentration-response curves of oxytocin alone and in the presence of verapamil (VER). VER significantly depressed (p <0.01) the Emax and shifted the curve to the right (n = 6 rats).

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