Key result
Iberiotoxin antagonized progesterone-induced inhibition of rat portal vein contractility, suggesting the suppression is mediated by the opening of BKCa channels.
Progesterone suppresses rat portal vein contractility via the opening of BKCa channels, an effect that can be specifically antagonized by iberiotoxin.
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Hypothesis-generating for BKCa mediation of progesterone's vascular effects in rats; leaves open translation to human physiology or therapy.
The suppression of contractility of rat portal vein caused by progesterone appears to be due to the potassium (K+) channel opening effect of this hormone. The identity of the specific K+ channels involved has been investigated using a variety of K+ channel blockers. Incubation with 100 nM iberiotoxin antagonised the progesterone-induced inhibition of spontaneous and 20 mM K+-induced phasic activity of the portal vein such that the contractions resembled those of the non-progesterone, non-iberiotoxin control tissues treated with the corresponding solvent vehicles. Incubation with barium chloride (20 and 100 microM), 4-aminopyridine (1 mM), tetraethylammonium chloride (1 mM), glibenclamide (1 microM) or apamin (1 microM) did not, however, have the same antagonistic effect. These results suggest that progesterone's selective suppression of rat portal vein contractility is mediated by the opening of BKCa channels.
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Mukerji et al. (2000) studied Progesterone-induced suppression of rat portal vein contractility. Potassium channel blockers (iberiotoxin) vs. Solvent vehicle controls was evaluated on Progesterone-induced inhibition of spontaneous and 20 mM K+-induced phasic activity. Iberiotoxin antagonized progesterone-induced inhibition of rat portal vein contractility, suggesting the suppression is mediated by the opening of BKCa channels.
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