选定的生物胺,包括微量胺,在大鼠离体灌注肠系膜血管网络中的差异血管加压作用

M. A. Anwar, W. R. Ford, K. J. Broadley
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引用次数: 0

摘要

肠系膜血管床的血管反应性调控尚不完全清楚。关于儿茶酚胺和5 -羟色胺对胰腺血管床的收缩反应有大量的信息,但关于微量胺如何影响血管张力的信息很少(1)。本研究的目的是比较选择的经典[去甲肾上腺素(NA)、甲氧沙明(M)、5 -羟色胺(S)]和微量胺[间辛phrine (SE, phenylephrine)、色胺(TRP),大鼠肠系膜循环中的酪胺(TYR)和-苯乙胺(B-PEA)。我们检验了微量胺的效力相对于其他单胺的假设。方法选取体重280 ~ 340 g的雄性Sprague-Dawley大鼠36只,采用震荡和颈椎脱位法处死。肠系膜上动脉插管,切除肠系膜动脉床,置于灌注室(2)。用克雷布斯碳酸氢盐溶液恒流量(4ml min-1)灌注床,加热至37℃,充气(5% CO2 in O2),最终pH 7.4。通过连接计算机数据采集系统(AD Instruments Powerlab图5)的压力传感器(Elcomatic em750)监测灌注压力。以100 μL体积注射的激动剂为剂量(0.01 ~ 1000 nmol),构建NA、M、S、SE、TRP、TYR和B-PEA的剂量-反应曲线。计算ED50(产生最大效应的一半所需的剂量,EMax)和EMax值,结果用mean±SEM表示,n为使用的动物数。结果单胺类药物的敏感性(ED50)依次为:S(2.9±0.6,n = 6) >NA(16.1±4.3,n = 6) = SE(20.2±4.6,n = 6)比;TRP(35.2±6.3,n = 6) = M(53.2±12.2,n = 5)。疗效(EMax)排序为:NA(162±20)= SE(139±5)= M(125±22)>S(51±6)= trp(38±3)。Tyr (n = 4)和B-PEA (n = 3)对大鼠肠系膜血管床均无收缩作用;然而,我们最近的研究表明,这两种分子在动脉网络中产生血管抑制反应(3)。产生肠系膜血管树剂量相关收缩的化合物增加血管阻力,因此可能调节动脉血压。然而,需要进一步的工作来描述最近克隆的微量胺相关受体(TAARs)与肠系膜循环中经典胺受体(如果有的话)产生的影响。同时,确定TAARs的作用机制,进一步明确TAARs在高血压和糖尿病等疾病中的生理和病理作用。其结果可能为治疗干预开辟新的途径。M.A.A.是惠康信托奖学金的接受者。格兰迪,D.K.(2007)。杂志。其他。, 116, 355-390。麦格雷戈博士(1965)。j .杂志。, 177, 21 - 30。布罗德利,K.J.等人(2008)。Br。j .减轻。11月19日至8日。
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Differential vasopressor actions of selected biogenic amines, including trace amines, in the rat isolated perfused mesenteric vascular network

Introduction

Regulation of vascular reactivity of the mesenteric vascular bed is not completely known. There is substantial information on contractile response to catecholamines and serotonin of the splanchnic vascular bed, but little information exists on how trace amines influence vascular tone (1). The purpose of the present investigation was to compare vasoconstrictor responses of selected classic [noradrenaline (NA), methoxamine (M), serotonin (S)] and trace amines [meta-synephrine (SE, phenylephrine), tryptamine (TRP), tyramine (TYR) and beta-phenylethylamine (B-PEA)] in the rat mesenteric circulation. We tested the hypothesis that potency of trace amines will be moderate compared to the other monoamines.

Method

Thirty-six male Sprague-Dawley rats (280–340 g body weight) were killed by concussion and cervical dislocation. The superior mesenteric artery was cannulated and the mesenteric arterial bed excised and placed in a perfusion chamber (2). The bed was perfused at a constant flow rate (4 mL min-1) with Krebs’ bicarbonate solution, warmed to 37°C and gassed (5% CO2 in O2), final pH 7.4. Perfusion pressure was monitored by means of a pressure transducer (Elcomatic EM 750) connected to a computer data acquisition system (AD Instruments Powerlab Chart 5).

Dose-response curves were constructed for NA, M, S, SE, TRP, TYR and B-PEA by bolus doses (range of 0.01–1000 nmoles) of agonists injected in a 100 μL volume. ED50 (the dose required to produce half of the maximum effect, EMax) and EMax values were calculated and results expressed as mean ± SEM, n represents the number of animals used.

Results

Sensitivity (ED50) of monoamines followed the order: S (2.9 ± 0.6, n = 6) > NA (16.1 ± 4.3, n = 6) = SE (20.2 ± 4.6, n = 6) > TRP (35.2 ± 6.3, n = 6) = M (53.2 ± 12.2, n = 5). The efficacy (EMax) sequence was of the rank order: NA (162 ± 20) = SE (139 ± 5) = M (125 ± 22) > S (51 ± 6) = TRP (38 ± 3). Both, Tyr (n = 4) and B-PEA (n = 3) yielded no vasoconstrictor effects on rat mesenteric vascular bed; however, we have recently shown that both of these molecules generate vasodepressor responses in this arterial network (3).

Discussion

Compounds producing dose-related contractions of the mesenteric vascular tree increase vascular resistance and hence may regulate arterial blood pressure. Nevertheless, additional work is warranted to delineate the effects produced at the recently cloned trace amine associated receptors (TAARs) from those, if any, of the classic amine receptors in the mesenteric circulation. Also, to determine their mechanism of action, and to further define the physiological and physiopathological (hypertension and diabetes) roles of TAARs. The outcome of which may open new avenues for therapeutic interventions.

Acknowledgements

M.A.A. was a recipient of a Wellcome Trust Fellowship.

References

Grandy, D.K. (2007). Pharmacol. Ther., 116, 355–390.

McGregor, D.D. (1965). J. Physiol.,177, 21–30.

Broadley, K.J. et al. (2008). Br. J. Nutr., Nov 19, e1–8.

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