The Effects of Potassium Channel Blockers on Progesterone-Induced Suppression of Rat Portal Vein Contractility
Authors: Mukerji M.S.1; Leathard H.L.1; Huddart H.2
Source: Journal of Pharmacy and Pharmacology, Volume 52, Number 8, 1 August 2000 , pp. 983-990(8)
Publisher: Pharmaceutical Press
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Abstract:
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.
Document Type: Research article
DOI: 10.1211/0022357001774705
Affiliations: 1: Department of Nursing Studies, St. Martin’s College, Lancaster LA1 3JD 2: Department of Biological Sciences, IENS, Lancaster University, Lancaster LA1 4YQ, UK
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