激活人类β1-上腺体受体的自身抗体与慢性心力衰竭中心脏功能降低有关
R Jahns1, V Boivin, C Siegmund
1Medizinische Poliklinik, Institut für Pharmakologie, University of Würzburg, Germany.
Circulation
|February 9, 1999
概括
针对β-上腺体受体的激活性自身抗体在扩张性心肌病患者中被发现. 这些自身抗体会损害受体功能,这表明它们在心力衰竭中起作用,并且可能是β-阻断剂的潜在治疗点.
科学领域:
- 心脏病学 心脏病学
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 对β-上腺体受体的自身抗体与心肌病有关.
- 之前的研究缺乏抗体与本地受体相互作用或临床影响的证据.
研究的目的:
- 调查针对β-上腺体受体的自身抗体是否与人类本地受体相互作用.
- 确定心肌病患者这种相互作用的临床意义.
主要方法:
- 选了104名心肌病患者和108名健康对照对抗beta受体的IgG抗体.
- 分析了与原生重组人类β-上腺素受体的抗体结合和功能相互作用.
- 评估了抗体患病率和与左心室功能相关的关系.
主要成果:
- 51%的患者具有与受体反应的抗体;只有一个子集识别了本地受体.
- 这些特定的自身抗体损害了受体连接体的结合,并增强了信号传递.
- 患病率为对照组的1%,缺血性心肌病的10%,扩张性心肌病的26%,与较差的心室功能有关.
结论:
- 对人类β-上腺体受体的激活性自身抗体存在于大约25%的扩张性心肌病患者中.
- 这些自身抗体会损害受体功能,并与左心室功能减弱有关.
- 阻断这些自身抗体可能有助于在心力衰竭中阻断β-上腺体受体的好处.
相关概念视频
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 Antagonists: Pharmacological Actions of β-Receptor Blockers
β-receptor blockers significantly impact the cardiovascular system by counteracting catecholamine-induced sympathetic responses. These medications decrease heart rate, contractility, and cardiac output, potentially leading to cardiac depression, life-threatening bradycardia, and death. Therapeutically, β-blockers function as mild antihypertensives and are utilized in treating angina pectoris and cardiac arrhythmias. However, nonselective β-blockers inhibit β2-receptors in bronchial smooth...
Antihypertensive Drugs: Action of β1 Blockers
β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this, β1-blockers...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Heart Failure Drugs: β-Blockers
β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
Heart Failure II: Pathophysiology
Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...


