Nicotine stimulation of the medulla increases blood flow of the common carotid artery in cats
| Autor: | Chi-Li Gong, Jon-Son Kuo, Yuk-Man Leung, Nai-Nu Lin, Tony Jer-Fu Lee |
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| Rok vydání: | 2009 |
| Předmět: |
Agonist
Male medicine.medical_specialty Nicotine Microinjections medicine.drug_class Carotid Artery Common Glutamic Acid Kainate receptor AMPA receptor Nicotinic Antagonists Receptors N-Methyl-D-Aspartate Choline Cellular and Molecular Neuroscience Receptors Kainic Acid Internal medicine medicine Animals Protein Isoforms Nicotinic Agonists Receptors AMPA Medulla Oblongata Dose-Response Relationship Drug Endocrine and Autonomic Systems Chemistry Glutamate receptor Hemodynamics Stimulation Chemical Nicotinic acetylcholine receptor Nicotinic agonist Endocrinology nervous system Regional Blood Flow Cats NMDA receptor Female Neurology (clinical) medicine.drug |
| Zdroj: | Autonomic neuroscience : basicclinical. 152(1-2) |
| ISSN: | 1872-7484 |
| Popis: | Microinjection of nicotine or glutamate into the dorsal facial area (DFA) of the medulla increases blood flow of common carotid artery (CCA). Whether there is a causal relationship between these two events is not known. Various agonists and antagonists for the nicotinic and glutamatergic receptors were microinjected through a four-barrel tubing into the DFA of anesthetized cats. Microinjections of nicotine [a non-selective nicotinic acetylcholine receptor (nAChR) agonist], choline (a selective alpha7-nAChR agonist), glutamate or KCl induced a modest increase in CCA blood flow. The nicotine- and choline-induced increases were reduced by alpha-bungarotoxin (an alpha7-nAChR antagonist) as well as MK-801 (a non-competitive NMDA receptor antagonist) or glutamate diethylester (a competitive AMPA/kainate receptor antagonist). The glutamate or KCl-induced increases were blocked by MK-801 and glutamate diethylester, but not by alpha-bungarotoxin. In conclusion, activation of nAChRs primarily via alpha7-nAChR caused a release of glutamate, which in turn activated NMDA and AMPA receptors, while cholinergic substance was not released into the DFA to activate the nicotinic receptor. |
| Databáze: | OpenAIRE |
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