Joyner W L, Mohama R E, Gilmore J P
Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha 68105-1065.
Microvasc Res. 1988 Jan;35(1):8-20. doi: 10.1016/0026-2862(88)90046-5.
The present study was undertaken to determine the specificity of the vasoconstrictor activity to angiotensin II (AII) and arginine vasopressin (AVP) on the microcirculation in normal and renovascular hypertensive states. Ten to fourteen days after the induction of hypertension, Syrian hamsters were anesthetized with pentobarbital sodium, the cheek pouch was exposed, and a plastic chamber was placed in situ so the membrane could be suffused with bicarbonate-buffered Ringer's solution (5% CO2, 95% N2, pH 7.4). Third order arterioles (30-45 micron) were identified for study and vessel diameter was measured using a shearing device. In one group of normotensive and hypertensive hamsters, AII was microapplied to the arteriole before and after adding an AVP antagonist to the suffusate. In a second group of similar hamsters, AVP was microapplied to the arteriole before and after adding an angiotensin II blocker, saralasin acetate, to the suffusate. AVP and AII receptor blockade was documented by observing whether the vasoconstrictor effect of either AVP or AII was abolished. Dose-response curves for either peptide were not altered in the presence of the antagonist to the other peptide; however, they were shifted to the left in the RHT hamsters. Neither AVP nor AII receptor blockade altered control resting arteriolar diameters. Thus, it can be concluded that the microvascular response to both AII and AVP are potentiated in RHT and there are no interactions between either AII or AVP with the receptors of the other peptide in these microvessels in normal or RHT hamsters, indicating a high specificity for each peptide to its vascular receptor.
本研究旨在确定血管紧张素II（AII）和精氨酸加压素（AVP）在正常和肾血管性高血压状态下对微循环的血管收缩活性的特异性。在诱导高血压10至14天后，用戊巴比妥钠麻醉叙利亚仓鼠，暴露颊囊，并在原位放置一个塑料腔室，以便用碳酸氢盐缓冲的林格氏液（5%二氧化碳，95%氮气，pH 7.4）灌注膜。识别出三级小动脉（30 - 45微米）进行研究，并使用剪切装置测量血管直径。在一组正常血压和高血压仓鼠中，在向灌注液中添加AVP拮抗剂之前和之后，将AII微量施加到小动脉上。在另一组类似的仓鼠中，在向灌注液中添加血管紧张素II阻滞剂醋酸沙拉新之前和之后，将AVP微量施加到小动脉上。通过观察AVP或AII的血管收缩作用是否被消除来记录AVP和AII受体阻断情况。在存在另一种肽的拮抗剂的情况下，任何一种肽的剂量 - 反应曲线均未改变；然而，在肾血管性高血压（RHT）仓鼠中它们向左移动。AVP和AII受体阻断均未改变对照时的静息小动脉直径。因此，可以得出结论，在RHT中对AII和AVP的微血管反应均增强，并且在正常或RHT仓鼠的这些微血管中，AII或AVP与另一种肽的受体之间没有相互作用，这表明每种肽对其血管受体具有高度特异性。
