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	<title>Translations:Calcium channel blocker/23/en - Revision history</title>
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	<updated>2026-05-11T09:50:45Z</updated>
	<subtitle>Revision history for this page on the wiki</subtitle>
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		<title>FuzzyBot: Importing a new version from external source</title>
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		<updated>2023-11-07T09:46:48Z</updated>

		<summary type="html">&lt;p&gt;Importing a new version from external source&lt;/p&gt;
&lt;p&gt;&lt;b&gt;New page&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Research indicates [[alcohol (drug)|ethanol]] is involved in the inhibition of L-type calcium channels. One study showed the nature of ethanol binding to L-type calcium channels is according to first-order kinetics with a [[Hill coefficient]] around 1. This indicates ethanol binds independently to the channel, expressing [[cooperative binding|noncooperative binding]]. Early studies showed a link between calcium and the release of [[vasopressin]] by the [[secondary messenger system]]. Vasopressin levels are reduced after the ingestion of alcohol. The lower levels of vasopressin from the consumption of alcohol have been linked to ethanol acting as an antagonist to voltage-gated calcium channels (VGCCs). Studies conducted by Treistman et al. in the [[aplysia]] confirm inhibition of VGCC by ethanol. [[Voltage clamp]] recordings have been done on the aplysia neuron. VGCCs were isolated and calcium current was recorded using [[patch clamp]] technique having ethanol as a treatment. Recordings were replicated at varying concentrations (0, 10, 25, 50, and 100 mM) at a voltage clamp of +30 mV. Results showed calcium current decreased as concentration of ethanol increased. Similar results have shown to be true in single-channel recordings from isolated nerve terminal of rats that ethanol does in fact block VGCCs.&lt;/div&gt;</summary>
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