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Kava or kava kava (Piper methysticum: Latin 'pepper' and Latinized Greek 'intoxicating') is a plant in the pepper family, native to the Pacific Islands. [1] The name kava is from Tongan and Marquesan, meaning 'bitter.’ [1] Other names for kava include ʻawa (), [2] ʻava (), yaqona or yagona (), [3] sakau (), [4] seka (), [5] and malok or malogu (parts of Vanuatu). [6]
Yangonin is one of the six major kavalactones found in the kava plant. [1] It has been shown to possess binding affinity for the cannabinoid receptor CB 1 (K i = 0.72 μM), and selectivity vs. the CB 2 receptor (K i >10 μM) where it behaves as an agonist.
Piper hooglandii, commonly known as kava, is a flowering plant in the family Piperaceae. The specific epithet honours Dutch botanist Ruurd Dirk Hoogland. [1] Description
The general structure of the kavalactones, without the R 1-R 2-O-CH 2-O- bridge and with all possible C=C double bonds shown.. Kavalactones are a class of lactone compounds found in kava roots and Alpinia zerumbet (shell ginger).
Piper hooglandii, endemic to Lord Howe Island, is locally known as "kava" Piper excelsum subsp. psittacorum, a subspecies of Piper excelsum is commonly known as "kava" Piper methysticum, commonly known as kava, can be used to make a drink with sedative and anesthetic properties
Papua New Guinea: Kava Pitcairn Islands: Ti' punch Samoa: Kava Solomon Islands: Kava Tokelau: Kava Tonga: Kava is a very important drink in Tonga, and some would also argue that it is their unofficial national drink. In Tonga, kava is like alcohol and drunk nightly at kalapu (Tongan for "club"), which is also called a faikava ("to do kava ...
Piper excelsum (formerly known as Macropiper excelsum) of the pepper family (Piperaceae) and commonly known as kawakawa, is a small tree of which the subspecies P. excelsum subsp. excelsum is endemic to New Zealand; [3] the subspecies P. e. subsp. psittacorum is found on Lord Howe Island, Norfolk Island and the Kermadec Islands.
Kavain has anticonvulsive properties, attenuating vascular smooth muscle contraction through interactions with voltage-dependent Na + and Ca 2+ channels. [1] How this effect is mediated, and to what extent this mechanism is involved in the anxiolytic and analgesic effects of kavalactones on the central nervous system, is unknown.