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Cellular target of voltage and calcium-dependent K(+) channel blockers involved in EDHF-mediated responses in rat superior mesenteric artery.

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Document type : Article de périodique (Journal article) – In Vitro, Journal Article, Research Support, Non-U.S. Gov't
Abstract :

1. We have investigated the cellular target of K(+) channel blockers responsible for the inhibition of the EDHF-mediated relaxation in the rat mesenteric artery by studying their effects on tension, smooth muscle cell (SMC) membrane potential and endothelial cell Ca(2+) signal ([Ca(2+)](endo)). 2. In arteries contracted with prostaglandin F(2 alpha) (2.5 - 10 microM), relaxation evoked by ACh (0.01 - 3 microM) was abolished by a combination of charybdotoxin (ChTX, 0.1 microM) plus apamin (Apa, 0.1 microM) and was inhibited by 68+/-6% (n=6) by 4-aminopyridine (4-AP, 5 mM). 3. ACh(0.001 - 3 microM) increased [Ca(2+)](endo) and hyperpolarized SMCs with the same potency, the pD(2) values were equal to 7.2+/-0.08 (n=4) and 7.2+/-0.07 (n=9), respectively. SMCs hyperpolarization to ACh (1 microM) was abolished by high K(+) solution or by ChTX/Apa. It was decreased by 66+/-5% (n=6) by 4-AP. 4. The increase in [Ca(2+)](endo) evoked by ACh (1 microM) was insensitive to ChTX/Apa but was depressed by 58+/-16% (n=6) and 27+/-4% (n=7) by raising external K(+) concentration and by 4-AP, respectively. 5. The effect of 4-AP on [Ca(2+)](endo) was not affected by increasing external K(+) concentration. In Ca-free/EGTA solution, the transient increase in [Ca(2+)](endo) evoked by ACh (1 microM) was abolished by thapsigargin (1 microM) and was decreased by 75+/-7% (n=5) by 4-AP. 6. These results show that inhibition of EDHF-evoked responses by 4-AP may be attributed to a decrease in the Ca(2+) release activated by ACh in endothelial cells. The abolition of SMCs hyperpolarization to ACh by ChTX/Apa is not related to an interaction with the [Ca(2+)](endo).
Access type : Accès libre
Publication date : 2001
Journal information : "British journal of pharmacology" - Vol. 134, no. 5, p. 1021-8 (2001)
Peer reviewed : yes
issn : 0007-1188
Publication status : Publié
Affiliation : UCL - MD/FSIO - Département de physiologie et pharmacologie
MESH Subject : 4-Aminopyridine - pharmacology ; Acetylcholine - pharmacology ; Animals ; Apamin - pharmacology ; Biological Factors - physiology ; Calcium - metabolism ; Calcium Signaling - drug effects ; Charybdotoxin - pharmacology ; Cytosol - drug effects - metabolism ; Dose-Response Relationship, Drug ; Endothelium, Vascular - cytology - drug effects - metabolism ; Male ; Membrane Potentials - drug effects ; Mesenteric Artery, Superior - drug effects - physiology ; Muscle, Smooth, Vascular - cytology - drug effects - physiology ; Potassium - pharmacology ; Potassium Channel Blockers - pharmacology ; Potassium Channels, Calcium-Activated - antagonists & inhibitors - physiology ; Rats ; Rats, Inbred WKY ; Vasodilation - drug effects ; Vasodilator Agents - pharmacology
Links :
Bibliographic reference Ghisdal, Philippe ; Morel, Nicole. Cellular target of voltage and calcium-dependent K(+) channel blockers involved in EDHF-mediated responses in rat superior mesenteric artery.. In: British journal of pharmacology, Vol. 134, no. 5, p. 1021-8 (2001)
Permanent URL http://hdl.handle.net/2078.1/8977

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