ヒトにおけるニューロンおよびアドレノメドゥラリ・カテキオラミンを放出する刺激の比較評価
Circulation
|April 1, 1979
まとめ
ナトリウム制限と運動は,交感神経からのノレピネフリン放出を増加させ,カフェインと運動は,副腎髄からのエピネフリン放出を刺激する. 異なる刺激により,これらのカテキオラミン反応が解離される.
科学分野:
- 神経科学は神経科学である.
- エンドクリノロジー エンドクリノロジー
- 生理学 生理学とは
背景:
- 交感神経系は,カテコアミンを通して,重要な生理学的機能を調節する.
- ニューロンのノルエピネフリンとアドレノメドラーエピネフリンは,異なる役割を持つ重要なカテキオラミンです.
- ストレス反応を理解するために,それらの異なる放出を理解することは極めて重要です.
研究 の 目的:
- ニューロンおよびアドレノメドラーカテキオラミンの差異的な放出を調査する.
- 交感神経系の構成要素を選択的に活性化する刺激を特定する.
- カテコロアミン濃度に対するナトリウム制限の影響を評価する.
主な方法:
- 血カテキオラミン (ノレピネフリン,エピネフリン) の測定.
- 尿中のカテキオラミン代謝産物 (ノルメタネフリン,メタネフリン) の定量化.
- ナトリウム制限,運動,オーソスタシス,カフェイン,冷圧テスト,ハンドグリップ,ヴァルサルバマニュバー,昏睡などの様々な交感神経系刺激の適用.
主要な成果:
- ナトリウム制限はプラズマのノルエピネフリンと尿中のノルメタネフリンを有意に増加させたが,エピネフリンやメタネフリンは増加しなかった.
- トレードミルの運動,オーソスタシス,カフェイン,冷圧テスト,ナトリウム制限,ハンドグリップ運動は,ノレピネフリン放出のための強力な刺激でした.
- カフェイン,トレッドミルの運動,冷圧テスト,ハンドグリップ運動,ヴァルサルバマニュアルはエピネフリン放出を増加させる.
- 昏睡はエピネフリンに顕著な影響を及ぼしたが,ノルエピネフリンレベルにはわずかな影響しか及ぼさなかった.
結論:
- 異なる刺激により,ヒトのニューロンおよびアドレノメデュラー源からカテキオラミン放出の異なるパターンが引き出されます.
- ニューロンのノレピネフリンとアドレノメドゥラルのエピネフリン放出の活性化の間には頻繁に解離があります.
- これらの発見は,交感神経系の規制の複雑さを強調しています.
さらに関連する動画
13:35A Convenient Method for Extraction and Analysis with High-Pressure Liquid Chromatography of Catecholamine Neurotransmitters and Their Metabolites
Published on: March 1, 2018
07:56A Plate-Based Assay for the Measurement of Endogenous Monoamine Release in Acute Brain Slices
Published on: August 11, 2021
関連する概念動画
01:27Adrenergic Neurons: Neurotransmission
Postganglionic sympathetic fibers (except those supplying the sweat glands) releasing noradrenaline or norepinephrine are called noradrenergic or adrenergic neurons. Noradrenaline, dopamine, adrenaline, or epinephrine are collectively called "catecholamines" as they contain a catechol moiety and an amine side chain. The five stages of neurotransmitter release involve their synthesis, storage, release, reuptake and metabolism.
Synthesis: Catecholamine synthesis requires tyrosine, which is taken...
Synthesis: Catecholamine synthesis requires tyrosine, which is taken...
01:27Adrenergic Receptors (Adrenoceptors): Classification
Adrenergic receptors, or adrenoceptors, respond to the autonomic neurotransmitter noradrenaline and other endogenous catecholamine agonists. They are classified into two main families, α and β, based on their pharmacological response and are further subdivided depending on their location, elicited response, and affinity to specific agonists or antagonists.
α-Adrenoceptors
α-Adrenoceptors are classified into two main subtypes: α1 and α2. The α1 adrenoceptors, which are found on postsynaptic...
α-Adrenoceptors
α-Adrenoceptors are classified into two main subtypes: α1 and α2. The α1 adrenoceptors, which are found on postsynaptic...
01:31Adrenergic Receptors: ɑ Subtype
Adrenoceptors are classified into α and ꞵ classes based on their potencies to catecholamine agonists. α-adrenoceptors show the following order of catecholamine potency:
Adrenaline ≥ Noradrenaline >> Isoprenaline
α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase C—inositol-1,4,5-trisphosphate...
Adrenaline ≥ Noradrenaline >> Isoprenaline
α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase C—inositol-1,4,5-trisphosphate...
01:26Adrenergic Receptors: β Subtype
β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors have equal affinities for...
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors have equal affinities for...
01:30Adrenergic Agonists: Direct-Acting Agents
Drugs that mimic the action of endogenous catecholamines like noradrenaline and adrenaline are called adrenergic agonists or sympathomimetics. Based on their mechanism of action, sympathomimetics can be classified as direct-, indirect-, or mixed-acting sympathomimetics. Direct-acting adrenergic agonists activate adrenoceptors without affecting presynaptic neurons, making them independent of neuronal catecholamine-depleting agents like reserpine and guanethidine.
These agents can be classified...
These agents can be classified...
01:25Adrenergic Agonists: Indirect-Acting Agents
Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...