The effects of potassium channel blockers on progesterone-induced suppression of rat portal vein contractility

The suppression of contractility of rat portal vein caused by progesterone appears to be due to the potassium (K+) channel opening effect of this horm one. The identity of the specific K+ channels involved has been investigate d using a variety of K+ channel blockers. Incubation with 100 nM iberiotoxin antagonised the progesterone-induced inh ibition of spontaneous and 20 mM K+-induced phasic activity of the portal v ein such that the contractions resembled those of the non-progesterone, non -iberiotoxin control tissues treated with the corresponding solvent vehicle s, Incubation with barium chloride (20 and 100 mu M), 4-aminopyridine (1 mM ), tetraethylammonium chloride (1 mM), glibenclamide (1 mu M) or apamin (1 mu M) did not, however, have the same antagonistic effect. These results suggest that progesterone's selective suppression of rat port al vein contractility is mediated by the opening of BKCa channels.