Sabourin T, Guay K, Houle S, Bouthillier J, Bachvarov D R, Adam A, Marceau F
Centre Hospitalier Universitaire de Québec, Centre de recherche du Pavillon l'Hôtel-Dieu de Québec, Québec (Québec), Canada, G1R 2J6.
Br J Pharmacol. 2001 Aug;133(7):1154-62. doi: 10.1038/sj.bjp.0704158.
The induction of B(1) receptors (B(1)Rs) and desensitization or down-regulation of B(2) receptors (B(2)Rs) as a consequence of the production of endogenous kinins has been termed the autoregulation hypothesis. The latter was investigated using two models based on the rabbit: kinin stimulation of cultured vascular smooth muscle cells (SMCs) and in vivo contact system activation (dextran sulphate intravenous injection, 2 mg kg(-1), 5 h). Rabbit aortic SMCs express a baseline population of B(1)Rs that was up-regulated upon interleukin-1beta treatment ([(3)H]-Lys-des-Arg(9)-BK binding or mRNA concentration evaluated by RT - PCR; 4 or 3 h, respectively). Treatment with B(1)R or B(2)R agonists failed to alter B(1)R expression under the same conditions. Despite consuming endogenous kininogen (assessed using the kinetics of immunoreactive kinin formation in the plasma exposed to glass beads ex vivo) and producing hypotension mediated by B(2)Rs in anaesthetized rabbits, dextran sulphate treatment failed to induce B(1)Rs in conscious animals (RT - PCR in several organs, aortic contractility). By contrast, lipopolysaccharide (LPS, 50 microg kg(-1), 5 h) was an effective B(1)R inducer (kidney, duodenum, aorta) but did not reduce kininogen reserve. We tested the alternate hypothesis that endogenous kinin participate in LPS induction of B(1)Rs. Kinin receptor antagonists (icatibant combined to B-9858, 50 microg kg(-1) of each) failed to prevent or reduce the effect of LPS on B(1)R expression. Dextran sulphate or LPS treatments did not persistently down-regulate vascular B(2)Rs (jugular vein contractility assessed ex vivo). The kinin receptor autoregulation hypothesis is not applicable to primary cell cultures derived from a tissue known to express B(1)Rs in a regulated manner (aorta). The activation of the endogenous kallikrein-kinin system is ineffective to induce B(1)Rs in vivo in an experimental time frame sufficient for B(1)R induction by LPS.
内源性激肽产生导致的B(1)受体(B(1)Rs)诱导以及B(2)受体(B(2)Rs)脱敏或下调被称为自身调节假说。使用基于兔子的两种模型对后者进行了研究:培养的血管平滑肌细胞(SMCs)的激肽刺激和体内接触系统激活(静脉注射硫酸葡聚糖,2 mg kg(-1),5小时)。兔主动脉平滑肌细胞表达基线水平的B(1)Rs,在白细胞介素-1β处理后上调(分别通过[(3)H]-Lys-去-Arg(9)-BK结合或RT-PCR评估mRNA浓度;分别为4或3小时)。在相同条件下,用B(1)R或B(2)R激动剂处理未能改变B(1)R表达。尽管消耗了内源性激肽原(通过体外暴露于玻璃珠的血浆中免疫反应性激肽形成的动力学评估)并在麻醉兔中产生了由B(2)Rs介导的低血压,但硫酸葡聚糖处理未能在清醒动物中诱导B(1)Rs(多个器官的RT-PCR、主动脉收缩性)。相比之下,脂多糖(LPS,50 μg kg(-1),5小时)是一种有效的B(1)R诱导剂(肾脏、十二指肠、主动脉),但并未减少激肽原储备。我们测试了另一种假说,即内源性激肽参与LPS诱导B(1)Rs。激肽受体拮抗剂(阿替班与B-9858联合使用,各50 μg kg(-1))未能预防或降低LPS对B(1)R表达的影响。硫酸葡聚糖或LPS处理并未持续下调血管B(2)Rs(体外评估颈静脉收缩性)。激肽受体自身调节假说不适用于源自已知以调节方式表达B(1)Rs的组织(主动脉)的原代细胞培养。在足以由LPS诱导B(1)Rs的实验时间范围内,内源性激肽释放酶-激肽系统的激活在体内诱导B(1)Rs无效。