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Kava Fact of the Day Sodium Channel Blocker?

The Kap'n

The Groggy Kaptain (40g)
KavaForums Founder
Sodium Channel Blocking Effects?

Hello kava lovers. Today we're going to take a look into the sodium channel blocking functions of kavalactones and what that might mean. Kavalactones are a group of compounds found in the kava plant (Piper methysticum), which has been traditionally used in the South Pacific for its sedative, anxiolytic, and analgesic properties. While the exact mechanisms of action of kavalactones are not fully understood, they are known to interact with various neurotransmitter systems and ion channels, including sodium channels.

Sodium channels are proteins found in cell membranes throughout the human body, which play a crucial role in allowing sodium ions to enter cells. Sodium ions are positively charged atoms that help to regulate the electrical activity of cells and the transmission of signals between nerve cells, muscles, and other tissues.

In nerve cells, sodium channels are particularly important for generating and propagating electrical impulses, which allow messages to be sent from one part of the body to another. When a nerve cell is stimulated, sodium channels open up, allowing sodium ions to rush into the cell, creating a temporary electrical charge. This charge then triggers nearby sodium channels to open up, creating a chain reaction that propagates the electrical impulse along the nerve cell.

Sodium channels are also important in muscle cells, where they help to regulate muscle contraction. When a muscle cell is stimulated by a nerve cell, sodium channels open up, allowing sodium ions to enter the cell and trigger a series of chemical reactions that ultimately result in the contraction of the muscle.

Sodium channel blockade effects of kavalactones:

  1. Inhibition of sodium channel activity:
    1. Kavalactones (Kavain and Methysticin) have been found to inhibit voltage-gated sodium channels, which play a critical role in the generation and propagation of action potentials in neurons. By blocking these channels, kavalactones may decrease neuronal excitability, contributing to their sedative, anxiolytic and topical numbing effects.
  2. Modulation of neurotransmitter release:
    1. Sodium channel blockade by kavalactones may also modulate the release of neurotransmitters, such as glutamate and GABA, by affecting presynaptic neuronal activity. This, in turn, could contribute to the overall effects of kava on the central nervous system.
  3. Analgesic effects:
    1. The blockade of sodium channels by kavalactones may contribute to their analgesic properties. By inhibiting the propagation of pain signals along peripheral nerves and within the central nervous system, kavalactones may help reduce pain perception.
  4. Muscle relaxation:
    1. Sodium channel blockade by kavalactones may also contribute to their muscle-relaxant effects. By reducing neuronal excitability and neurotransmitter release, kavalactones can decrease the activity of motor neurons, leading to muscle relaxation.

It is important to remember that kavalactones may interact with other ion channels and neurotransmitter systems as well, and their effects are likely the result of multiple mechanisms of action. Additionally, and more like “traditionally”, more research is needed to fully elucidate the effects of kavalactones on sodium channels and their overall impact on the nervous system.

Note: One way in which we can clearly discern that kava inhibits sodium channels is through the numbing sensation we experience in our mouths when we drink it.

Sources:

Armstrong, Scott A., and Michael J. Herr. 2021. “Physiology, Nociception.” In StatPearls. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/pubmed/31855389.

Raduege, Kevin M., James F. Kleshinski, J. Victor Ryckman, and John E. Tetzlaff. 2004. “Anesthetic Considerations of the Herbal, Kava.” Journal of Clinical Anesthesia 16 (4): 305–11. https://doi.org/10.1016/j.jclinane.2003.08.009.

Eijkelkamp, Niels, John E. Linley, Mark D. Baker, Michael S. Minett, Roman Cregg, Robert Werdehausen, François Rugiero, and John N. Wood. 2012. “Neurological Perspectives on Voltage-Gated Sodium Channels.” Brain: A Journal of Neurology 135 (Pt 9): 2585–2612. https://doi.org/10.1093/brain/aws225.

Jamieson, D. D., and P. H. Duffield. 1990. “The Antinociceptive Actions of Kava Components in Mice.” Clinical and Experimental Pharmacology & Physiology 17 (7): 495–507. https://doi.org/10.1111/j.1440-1681.1990.tb01349.x.

Magura, E. I., M. V. Kopanitsa, J. Gleitz, T. Peters, and O. A. Krishtal. 1997. “Kava Extract Ingredients, ( )-Methysticin and (±)-Kavain Inhibit Voltage-Operated Na -Channels in Rat CA1 Hippocampal Neurons.” Neuroscience. https://doi.org/10.1016/s0306-4522(97)00177-2.

Mantegazza, Massimo, Giulia Curia, Giuseppe Biagini, David S. Ragsdale, and Massimo Avoli. 2010. “Voltage-Gated Sodium Channels as Therapeutic Targets in Epilepsy and Other Neurological Disorders.” Lancet Neurology 9 (4): 413–24. https://doi.org/10.1016/S1474-4422(10)70059-4.

Raduege, Kevin M., James F. Kleshinski, J. Victor Ryckman, and John E. Tetzlaff. 2004. “Anesthetic Considerations of the Herbal, Kava.” Journal of Clinical Anesthesia 16 (4): 305–11. https://doi.org/10.1016/j.jclinane.2003.08.009.

Singh, Yadhu N., and Nirbhay N. Singh. 2002. “Therapeutic Potential of Kava in the Treatment of Anxiety Disorders.” CNS Drugs 16 (11): 731–43. https://doi.org/10.2165/00023210-200216110-00002.

Singh, Yadhu N. 2009. “Kava: An Old Drug in a New World.” Cultural Critique 71 (1): 107–28. https://doi.org/10.1353/cul.0.0029.

Sula, Altin, Jennifer Booker, Leo C. T. Ng, Claire E. Naylor, Paul G. DeCaen, and B. A. Wallace. 2017. “The Complete Structure of an Activated Open Sodium Channel.” Nature Communications 8 (February): 14205. https://doi.org/10.1038/ncomms14205.

Sarris, Jerome, Emma LaPorte, and Isaac Schweitzer. 2011. “Kava: A Comprehensive Review of Efficacy, Safety, and Psychopharmacology.” The Australian and New Zealand Journal of Psychiatry 45 (1): 27–35. https://doi.org/10.3109/00048674.2010.522554.

Tikhonov, Denis B., and Boris S. Zhorov. 2017. “Mechanism of Sodium Channel Block by Local Anesthetics, Antiarrhythmics, and Anticonvulsants.” The Journal of General Physiology 149 (4): 465–81. https://doi.org/10.1085/jgp.201611668.

Yu, Frank H., and William A. Catterall. 2003. “Overview of the Voltage-Gated Sodium Channel Family.” Genome Biology 4 (3): 207. https://doi.org/10.1186/gb-2003-4-3-207.
 

JohnMichael

Kava Synchronized
Sodium Channel Blocking Effects?

Hello kava lovers. Today we're going to take a look into the sodium channel blocking functions of kavalactones and what that might mean. Kavalactones are a group of compounds found in the kava plant (Piper methysticum), which has been traditionally used in the South Pacific for its sedative, anxiolytic, and analgesic properties. While the exact mechanisms of action of kavalactones are not fully understood, they are known to interact with various neurotransmitter systems and ion channels, including sodium channels.

Sodium channels are proteins found in cell membranes throughout the human body, which play a crucial role in allowing sodium ions to enter cells. Sodium ions are positively charged atoms that help to regulate the electrical activity of cells and the transmission of signals between nerve cells, muscles, and other tissues.

In nerve cells, sodium channels are particularly important for generating and propagating electrical impulses, which allow messages to be sent from one part of the body to another. When a nerve cell is stimulated, sodium channels open up, allowing sodium ions to rush into the cell, creating a temporary electrical charge. This charge then triggers nearby sodium channels to open up, creating a chain reaction that propagates the electrical impulse along the nerve cell.

Sodium channels are also important in muscle cells, where they help to regulate muscle contraction. When a muscle cell is stimulated by a nerve cell, sodium channels open up, allowing sodium ions to enter the cell and trigger a series of chemical reactions that ultimately result in the contraction of the muscle.

Sodium channel blockade effects of kavalactones:

  1. Inhibition of sodium channel activity:
    1. Kavalactones (Kavain and Methysticin) have been found to inhibit voltage-gated sodium channels, which play a critical role in the generation and propagation of action potentials in neurons. By blocking these channels, kavalactones may decrease neuronal excitability, contributing to their sedative, anxiolytic and topical numbing effects.
  2. Modulation of neurotransmitter release:
    1. Sodium channel blockade by kavalactones may also modulate the release of neurotransmitters, such as glutamate and GABA, by affecting presynaptic neuronal activity. This, in turn, could contribute to the overall effects of kava on the central nervous system.
  3. Analgesic effects:
    1. The blockade of sodium channels by kavalactones may contribute to their analgesic properties. By inhibiting the propagation of pain signals along peripheral nerves and within the central nervous system, kavalactones may help reduce pain perception.
  4. Muscle relaxation:
    1. Sodium channel blockade by kavalactones may also contribute to their muscle-relaxant effects. By reducing neuronal excitability and neurotransmitter release, kavalactones can decrease the activity of motor neurons, leading to muscle relaxation.

It is important to remember that kavalactones may interact with other ion channels and neurotransmitter systems as well, and their effects are likely the result of multiple mechanisms of action. Additionally, and more like “traditionally”, more research is needed to fully elucidate the effects of kavalactones on sodium channels and their overall impact on the nervous system.

Note: One way in which we can clearly discern that kava inhibits sodium channels is through the numbing sensation we experience in our mouths when we drink it.

Sources:

Armstrong, Scott A., and Michael J. Herr. 2021. “Physiology, Nociception.” In StatPearls. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/pubmed/31855389.

Raduege, Kevin M., James F. Kleshinski, J. Victor Ryckman, and John E. Tetzlaff. 2004. “Anesthetic Considerations of the Herbal, Kava.” Journal of Clinical Anesthesia 16 (4): 305–11. https://doi.org/10.1016/j.jclinane.2003.08.009.

Eijkelkamp, Niels, John E. Linley, Mark D. Baker, Michael S. Minett, Roman Cregg, Robert Werdehausen, François Rugiero, and John N. Wood. 2012. “Neurological Perspectives on Voltage-Gated Sodium Channels.” Brain: A Journal of Neurology 135 (Pt 9): 2585–2612. https://doi.org/10.1093/brain/aws225.

Jamieson, D. D., and P. H. Duffield. 1990. “The Antinociceptive Actions of Kava Components in Mice.” Clinical and Experimental Pharmacology & Physiology 17 (7): 495–507. https://doi.org/10.1111/j.1440-1681.1990.tb01349.x.

Magura, E. I., M. V. Kopanitsa, J. Gleitz, T. Peters, and O. A. Krishtal. 1997. “Kava Extract Ingredients, ( )-Methysticin and (±)-Kavain Inhibit Voltage-Operated Na -Channels in Rat CA1 Hippocampal Neurons.” Neuroscience. https://doi.org/10.1016/s0306-4522(97)00177-2.

Mantegazza, Massimo, Giulia Curia, Giuseppe Biagini, David S. Ragsdale, and Massimo Avoli. 2010. “Voltage-Gated Sodium Channels as Therapeutic Targets in Epilepsy and Other Neurological Disorders.” Lancet Neurology 9 (4): 413–24. https://doi.org/10.1016/S1474-4422(10)70059-4.

Raduege, Kevin M., James F. Kleshinski, J. Victor Ryckman, and John E. Tetzlaff. 2004. “Anesthetic Considerations of the Herbal, Kava.” Journal of Clinical Anesthesia 16 (4): 305–11. https://doi.org/10.1016/j.jclinane.2003.08.009.

Singh, Yadhu N., and Nirbhay N. Singh. 2002. “Therapeutic Potential of Kava in the Treatment of Anxiety Disorders.” CNS Drugs 16 (11): 731–43. https://doi.org/10.2165/00023210-200216110-00002.

Singh, Yadhu N. 2009. “Kava: An Old Drug in a New World.” Cultural Critique 71 (1): 107–28. https://doi.org/10.1353/cul.0.0029.

Sula, Altin, Jennifer Booker, Leo C. T. Ng, Claire E. Naylor, Paul G. DeCaen, and B. A. Wallace. 2017. “The Complete Structure of an Activated Open Sodium Channel.” Nature Communications 8 (February): 14205. https://doi.org/10.1038/ncomms14205.

Sarris, Jerome, Emma LaPorte, and Isaac Schweitzer. 2011. “Kava: A Comprehensive Review of Efficacy, Safety, and Psychopharmacology.” The Australian and New Zealand Journal of Psychiatry 45 (1): 27–35. https://doi.org/10.3109/00048674.2010.522554.

Tikhonov, Denis B., and Boris S. Zhorov. 2017. “Mechanism of Sodium Channel Block by Local Anesthetics, Antiarrhythmics, and Anticonvulsants.” The Journal of General Physiology 149 (4): 465–81. https://doi.org/10.1085/jgp.201611668.

Yu, Frank H., and William A. Catterall. 2003. “Overview of the Voltage-Gated Sodium Channel Family.” Genome Biology 4 (3): 207. https://doi.org/10.1186/gb-2003-4-3-207.
Very, very interesting. Thanks!
 
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