Comparative nasal effects of bradykinin, kallidin and [Des‐Arg9]‐bradykinin in atopic rhinitic and normal volunteers.
Comparative nasal effects of bradykinin, kallidin and [Des‐Arg9]‐bradykinin in atopic rhinitic and normal volunteers.
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缓激肽、激肽和 [Des-Arg9]-缓激肽对特应性鼻炎和正常志愿者的鼻部影响的比较。
DOI：
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
P. Howarth
中科院分区：
文献类型：
--
作者：
K. Rajakulasingam;R. Polosa;S. Holgate;P. Howarth
1. 在特应性鼻炎（n = 7）和非鼻炎（n = 7）受试者中研究了鼻子内激肽的结构-活性关系。在一项双盲比较研究中，受试者在4天内随机接受递增剂量的B1激动剂[Des - Arg9] -缓激肽，B2激动剂kallidin或缓激肽，或对照安慰剂的鼻腔刺激。客观上采用主动后鼻测压法测量鼻气道阻力（NAR），主观上采用鼻塞、鼻流、鼻痒、鼻痛等症状报告监测鼻反应。2. 与安慰剂相比，B2激动剂kallidin和bradykinin均诱导NAR的剂量依赖性增加（P < 0.001），并且与鼻塞（P < 0.05）、鼻流（P < 0.01）和鼻不适（P < 0.05）的症状报告相关。相比之下，B1受体激动剂[Des‐Arg9]‐缓激肽对NAR和症状报告的影响与安慰剂没有区别。鼻炎患者和非鼻炎患者鼻腔对碱性肽和缓激肽的反应没有差异，也没有证据表明B1受体在疾病状态下上调。对于整个组，诱导NAR （PD50）增加50%的激动剂的刺激剂量为慢激肽1.77 × 10（‐4）mol，钾素2.86 × 10（‐4）mol （P > 0.05）。3. 这些发现表明，激肽的鼻腔作用是通过B2受体介导的，B2受体拮抗剂的出现将允许进一步评估激肽在鼻炎中的作用。
1. The structure‐activity relationship of kinins within the nose has been investigated in atopic rhinitic (n = 7) and non‐rhinitic (n = 7) subjects. On 4 separate days, each separated by a week, subjects randomly underwent nasal challenge with incremental doses of either the B1 agonist [Des‐Arg9]‐bradykinin, the B2 agonists kallidin or bradykinin, or vehicle placebo in a double‐blind comparative study. The nasal response was monitored objectively by measurement of nasal airways resistance (NAR) by active posterior rhinomanometry and subjectively by symptom reporting of nasal blockage, rhinorrhoea, nasal itch and nasal pain. 2. The B2 agonists kallidin and bradykinin both induced a dose‐dependent increase in NAR (P less than 0.001) and were associated with symptomatic reporting of nasal blockage (P less than 0.05), rhinorrhoea (P less than 0.01) and nasal discomfort (P less than 0.05) compared to placebo. In contrast the effects of the B1 agonist [Des‐Arg9]‐bradykinin on NAR and symptom reporting were indistinguishable from placebo. No difference could be identified in the nasal response to kallidin and bradykinin between rhinitic and non‐rhinitic subjects and there was no evidence of B1 receptor upregulation in the disease state. For the whole group the provocative dose of agonist inducing a 50% increase in NAR (PD50) was 1.77 x 10(‐4) mol for bradykinin and 2.86 x 10(‐4) mol for kallidin (P greater than 0.05). 3. These findings identify that the nasal effects of kinins are mediated through B2 receptors and the advent of B2 receptor antagonists will permit a further evaluation of the role of kinins in rhinitis.
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DOI：
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发表时间：
1985
期刊：
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影响因子：
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DOI：
10.1152/jappl.1982.53.4.985
发表时间：
1982
期刊：
Journal of applied physiology: respiratory, environmental and exercise physiology
影响因子：
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作者：
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DOI：
10.1152/ajprenal.1985.248.1.f48
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激肽是在过敏个体的鼻气道受到过敏原刺激后在体内产生的。
DOI：
10.1172/jci111127
发表时间：
1983
期刊：
The Journal of clinical investigation
影响因子：
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作者：
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