Cicletanine-Induced Decreases in Cytosolic Ca2+ Level and Contraction in Vascular Smooth Muscle.

Izumi Masanori, Mitsui-Saito Minori, Ozaki Hiroshi, Karaki Hideaki

doi:10.1254/jjp.76.57

The mechanism by which cicletanine (3-(4-chlorophenyl)-1, 3-dihydro-7-hydroxy-6-methylfuro-[3, 4-c]pyridine) induces vasodilatation was examined in isolated vascular smooth muscle. Cicletanine inhibited the contraction induced by high K⁺, norepinephrine (NE) and prostaglandin F_2α in a concentration-dependent manner in rat aorta. High K⁺ (15.8 – 72.7 mM) elicited elevation of cytosolic Ca²⁺ level ([Ca²⁺]_i) and contraction in a concentration-dependent manner. Cicletanine (300 μM) inhibited the high K⁺-induced contractions without changing the [Ca²⁺]_i/tension relationship. NE (3 – 300 nM) elicited greater contractions than high K⁺ at a given [Ca²⁺]_i, suggesting that NE increased Ca²⁺ sensitivity of the contractile elements. Cicletanine inhibited the NE-induced contractions without changing the slope of the [Ca²⁺]_i/tension relationship. Cicletanine inhibited the transient increases in both [Ca²⁺]_i and muscle tension elicited by NE but not the transient increase in [Ca²⁺]_i elicited by caffeine in Ca²⁺-free solution. Cicletanine did not inhibit contraction induced by Ca²⁺ in the permeabilized rabbit mesenteric artery with α-toxin. These results suggest that cicletanine inhibits vascular smooth muscle contraction by multiple mechanisms: 1) inhibition of Ca²⁺ influx via voltage-dependent Ca²⁺ channel and 2) inhibition of Ca²⁺ release mediated by the α-adrenoceptors, but not by caffeine.

Cicletanine-Induced Decreases in Cytosolic Ca2+ Level and Contraction in Vascular Smooth Muscle.

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Cicletanine-Induced Decreases in Cytosolic Ca2+ Level and Contraction in Vascular Smooth Muscle.

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