Abstract
1. It has been reported that omega-conotoxin GVIA (omega-CgTx) blocks L- and N-type voltage-sensitive Ca2+ channels (VSCCs) in neurones and inhibits neurotransmitter release in various tissues. The present study investigates the effects of omega-CgTx on electrical field stimulation (EFS)- and agonist-induced changes in free cytosolic Ca2+ ([Ca2+]cyt) levels and tension in isolated fura-2 loaded rat anococcygeus muscle. 2. EFS produced frequency-dependent increases in [Ca+]cyt levels and contractions. Phentolamine (1 microM) and omega-CgTx (0.1 microM) significantly inhibited EFS-induced responses and shifted the frequency-response curves to the right. 3. alpha-adrenoceptor agonists (noradrenaline and clonidine) and carbachol (in the presence of phentolamine) produced concentration-dependent increases in [Ca2+]cyt levels and contractions. Though omega-CgTx (0.1 microM) significantly inhibited the increases in [Ca2+]cyt levels induced by low doses of noradrenaline, the overall concentration-response curves of [Ca2+]cyt and contractions for noradrenaline, clonidine, and carbachol were not affected by omega-CgTx. 4. When the tone of rat anococcygeus muscle was raised with either clonidine (0.1 microM) or carbachol (30 microM, in the presence of 3 microM phentolamine), EFS (2 Hz) produced reproducible decreases in [Ca2+]cyt levels and relaxations. These responses were significantly inhibited by omega-CgTx when the tissue was precontracted with clonidine, but not when it was precontracted with carbachol. 5. The results of the present study suggest that in rat anococcygeus muscle, omega-CgTx inhibits the EFS-induced release of both excitatory and inhibitory neurotransmitters, probably by blocking Ca2+ channels on nerve terminals. Furthermore, the Ca2+ channels present on the smooth muscle cell membrane, which are involved in the agonist-induced Ca2+ influx and contractions, may not be sensitive to omega-CgTx.
Published Version
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