Research output: Contribution to Journal/Magazine › Journal article › peer-review
Research output: Contribution to Journal/Magazine › Journal article › peer-review
}
TY - JOUR
T1 - The Effects of Potassium Channel Blockers on Progesterone-Induced Suppression of Rat Portal Vein Contractility.
AU - Mukerji, M. S.
AU - Leathard, H. L.
AU - Huddart, Henry
PY - 2000/8
Y1 - 2000/8
N2 - 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 M), 4-aminopyridine (1 mM), tetraethylammonium chloride (1 mM), glibenclamide (1 M) or apamin (1 M) 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.
AB - 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 M), 4-aminopyridine (1 mM), tetraethylammonium chloride (1 mM), glibenclamide (1 M) or apamin (1 M) 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.
U2 - 10.1211/0022357001774705
DO - 10.1211/0022357001774705
M3 - Journal article
VL - 52
SP - 983
EP - 990
JO - Journal of Pharmacy and Pharmacology
JF - Journal of Pharmacy and Pharmacology
SN - 0022-3573
IS - 8
ER -