ジョージ・E・ブラウン記念講演会 ジョージ・E・ブラウン記念講演 アドレナージック神経伝送の局所調節
Circulation
|October 1, 1981
まとめ
シンパティック・ニューロエフェクターの交差点にある局所的要因は,ノレピネフリン放出を微調整し,心血管反射や血流調節に影響を与えます. これらのメカニズムは,局所性高血症と血管の同情的制御を理解するために不可欠です.
科学分野:
- 神経科学は神経科学である.
- 心血管生理学 心血管の生理学
- 薬理学 薬理学とは
背景:
- 心血管反射は,交感神経の活動とノレピネフリン放出を調節する.
- 交感性ニューロエフェクターの交差点は,神経伝達物質の可用性を調節するために重要である.
- 局所的な代謝変化やその他の要因は,交感神経伝達に影響を与えます.
研究 の 目的:
- ノルエピネフリン放出を調節する同情神経効果因子交差点の局所的な出来事をレビューする.
- これらの局所的な調節機構の生理学的意義について議論する.
- これらの神経効果因子相互作用の潜在的な臨床的重要性を調査する.
主な方法:
- 交感性ニューロエフェクター結合機能に関する既存の文献のレビュー.
- ノルエピネフリン放出と受容体の活性化に影響する要因の分析.
- 生理学的および薬理学的調節器に関する議論.
主要な成果:
- メタボリックの変化 (pHの低下,ハイポスモラリティ,K+の増加,アデノシン) はノレピネフリン放出を抑制する.
- アデノシン (adenosine) は,交感制御を減少させることで局所性高血症を媒介する.
- アセチルコリン,ヒスタミン,セロトニン,アンジオテンシンII,および温度などの他の物質も,ノルエピネフリン放出と受容体の活性を調節します.
結論:
- 交感神経効果因子の交差点にある局所的要因は,交感神経の活動と血流の調節に重要な役割を果たします.
- これらのメカニズムを理解することは,局所性高血症と血管制御を理解するために不可欠です.
- これらの局所的なイベントは,心臓血管疾患における潜在的な臨床的影響を及ぼします.
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関連する概念動画
Adrenergic 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...
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Adrenergic 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...
Adrenergic 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...
Adrenergic 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...
Adrenergic 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...
Adrenergic 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...
