ALPHA ADRENERGIC REGULATION OF AIRWAY BLOOD FLOW
气道血流的 ALPHA 肾上腺素调节
基本信息
- 批准号:2865284
- 负责人:
- 金额:$ 17.28万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1998
- 资助国家:美国
- 起止时间:1998-04-01 至 2001-03-31
- 项目状态:已结题
- 来源:
- 关键词:active immunization allergens alpha adrenergic agent alpha adrenergic receptor asthma bronchomotion calcium flux clinical research cyclic AMP diagnostic respiratory lavage glucocorticoids human subject inflammation laboratory rabbit norepinephrine protein kinase C receptor expression respiratory circulation respiratory hypersensitivity tissue /cell culture vascular endothelium vascular smooth muscle vasomotion
项目摘要
DESCRIPTION (Adapted from the applicant's abstract): Asthma is considered
to be an inflammatory airway disease. The airway circulation is therefore
likely to participate in some of its manifestations including exercise
induced bronchoconstriction, airway wall edema and the clearance of locally
released spasmogens. However, in contrast to airway smooth muscle
responsiveness, information on the effect of inflammation on airway vascular
smooth muscle responsiveness is lacking. The airway vasculature is part of
the systemic circulation and norepinephrine (NE) is the principal
neurotransmitter for the local adrenergic regulation of airway blood flow.
In recent studies, the principal investigator has shown that asymptomatic
asthmatics have an exaggerated vasoconstrictor response in the airway to an
inhaled adrenergic agonist and that repeated antigen challenge potentiates
NE-induced contraction of small bronchial arterial rings in sensitized
rabbits. These observations indicated that inflammation causes
alpha-adrenergic hyperresponsiveness of the airway vasculature, possibly as
an adaptive mechanism to counteract inflammatory vasodilation. The present
proposal is based on the hypothesis that the inflammatory increase in
alpha-adrenergic vascular responsiveness is due to upregulated
alpha-adrenergic signaling in vascular smooth muscle or decreased
alpha-adrenergic generation of endothelial relaxing factors, or both. This
will be tested by 1) assessing the effects of short-term and long-term
inflammatory stimulation on alpha1 and alpha2-receptor expression and
adrenergic signal transduction in rabbit bronchial arterial smooth muscle
and in endothelium, 2) correlating these findings with NE-induced bronchial
arterial contraction and its endothelial modulation, 3) comparing
alpha-adrenergic responsiveness of airway blood flow between asthmatics and
normals, and 4) determining the effect of glucocorticosteroids on enhanced
alpha-adrenergic responsiveness. These experiments are expected to yield
new information on the regulation of the airway circulation in bronchial
asthma and possibly identify novel therapeutic approaches.
描述(改编自申请人摘要):考虑哮喘
是一种炎症性气道疾病 因此,
有可能参与其某些表现形式,包括运动
诱导支气管收缩,气道壁水肿和清除局部
释放了痉挛素 然而,与气道平滑肌相比,
反应性,关于炎症对气道血管的影响的信息
缺乏平滑肌反应性。 气道脉管系统是
体循环和去甲肾上腺素(NE)是主要的
神经递质,用于气道血流的局部肾上腺素能调节。
在最近的研究中,主要研究者表明,
哮喘患者在气道中具有对哮喘的过度的血管收缩反应,
吸入肾上腺素能激动剂和重复抗原激发增强
NE引起致敏大鼠支气管小动脉环收缩
家兔 这些观察结果表明,炎症导致
气道血管系统的α肾上腺素能高反应性,可能是因为
对抗炎症性血管舒张的适应性机制。 本
该提案是基于这样的假设,即炎症的增加,
α-肾上腺素能血管反应性是由于
血管平滑肌中的α-肾上腺素能信号传导或降低
内皮松弛因子的α-肾上腺素能生成,或两者。 这
将通过1)评估短期和长期的影响进行测试
炎症刺激对α 1和α 2受体表达的影响,
兔支气管动脉平滑肌肾上腺素能信号转导
2)将这些发现与NE诱导的支气管炎相关,
动脉收缩及其内皮调节,3)比较
哮喘患者和哮喘患者气道血流的α肾上腺素能反应性
正常人,以及4)确定糖皮质激素对增强的
α-肾上腺素能反应 这些实验有望产生
支气管哮喘气道循环调节的新信息
并可能发现新的治疗方法。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Adam Wanner其他文献
Adam Wanner的其他文献
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{{ truncateString('Adam Wanner', 18)}}的其他基金
ALPHA ADRENERGIC REGULATION OF AIRWAY BLOOD FLOW
气道血流的 ALPHA 肾上腺素调节
- 批准号:
2901299 - 财政年份:1998
- 资助金额:
$ 17.28万 - 项目类别:
ALPHA-ADRENERGIC REGULATION OF AIRWAY BLOOD FLOW
气道血流的α-肾上腺素调节
- 批准号:
2471560 - 财政年份:1998
- 资助金额:
$ 17.28万 - 项目类别:
ALPHA ADRENERGIC REGULATION OF AIRWAY BLOOD FLOW
气道血流的 ALPHA 肾上腺素调节
- 批准号:
6183929 - 财政年份:1998
- 资助金额:
$ 17.28万 - 项目类别:
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