ArticleThe Journal of general physiology1989
Influence of pHo on calcium channel block by amlodipine, a charged dihydropyridine compound. Implications for location of the dihydropyridine receptor.
Article in The Journal of general physiology, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 96 citations in OpenAlex.
- L-type calcium channel blockers at therapeutic concentrations are not linked to CRAC channels and heart failure.Clinical and experimental hypertension (New York, N.Y. : 1993) · 2025Article
- Structural biology of voltage-gated calcium channels.Channels (Austin, Tex.) · 2024Review
- Structural Basis of the Modulation of the Voltage-Gated Calcium Ion Channel CaAngewandte Chemie (International ed. in English) · 2021Article
- Distinct properties of amlodipine and nicardipine block of the voltage-dependent Ca2+ channels Cav1.2 and Cav2.1 and the mutant channels Cav1.2/dihydropyridine insensitive and Cav2.1/dihydropyridine sensitive.European journal of pharmacology · 2011Article
- Structural model for dihydropyridine binding to L-type calcium channels.The Journal of biological chemistry · 2009Article
- Location of KCNE1 relative to KCNQ1 in the I(KS) potassium channel by disulfide cross-linking of substituted cysteines.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Molecular mechanisms of vasoselectivity of the 1,4-dihydropyridine lercanidipine.British journal of pharmacology · 2004Article
- Construction of a high-affinity receptor site for dihydropyridine agonists and antagonists by single amino acid substitutions in a non-L-type Ca2+ channel.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Modulation by extracellular ATP of L-type calcium channels in guinea-pig single sinoatrial nodal cell.British journal of pharmacology · 1996Article
- Interactions between H+ and Ca2+ near cardiac L-type calcium channels: evidence for independent channel-associated binding sites.Biophysical journal · 1993Article
- The action of amlodipine on voltage-operated calcium channels in vascular smooth muscle.British journal of pharmacology · 1993Article
- Lacidipine, a new long-acting dihydropyridine calcium antagonist, has high vascular selectivity against all intracardiac variables.Heart and vessels · 1993Article
- Dihydropyridine receptor of L-type Ca2+ channels: identification of binding domains for [3H](+)-PN200-110 and [3H]azidopine within the alpha 1 subunit.Proceedings of the National Academy of Sciences of the United States of America · 1991Article
- Identification of 1,4-dihydropyridine binding regions within the alpha 1 subunit of skeletal muscle Ca2+ channels by photoaffinity labeling with diazipine.Proceedings of the National Academy of Sciences of the United States of America · 1991Article
- Article
- The interactions of 1,4-dihydropyridines bearing a 2-(2-aminoethylthio)methyl substituent at voltage-dependent Ca2+ channels of smooth muscle, cardiac muscle and neuronal tissues.Naunyn-Schmiedeberg's archives of pharmacologyArticle
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2 authors at 1 institution in 1 country.
Funding
Abstract
We have investigated the modulation of L-type calcium channel currents in isolated ventricular cells by the dihydropyridine derivative amlodipine, a weak base with a pKa of 8.6. Under conditions that favor neutral drug molecules, amlodipine block resembles other, previously described, neutral dihydropyridine derivatives: block is more pronounced at depolarized voltages, repetitive pulsing is not needed to promote block, and recovery is complete at hyperpolarized voltages. When the drug is ionized, depolarized voltages still enhance block, however, the time course is slow and speeded by repetitive pulses that open channels. Recovery from block by ionized drug molecules is very slow and incomplete, but can be rapidly modified by changes in external hydrogen ion concentration. We conclude from these observations that the degree of ionization of the drug molecule can affect access to the dihydropyridine receptor and that external protons can interact with the drug-receptor complex even if channels are blocked and closed. These observations place limitations on the location of this receptor in the ventricular cell membrane.
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