论文部分内容阅读
通过观察肾动脉主干张开角的大小，研究了自发性高血压大鼠（Spontaneouslyhypertensiverat，SHR）高血压建立前后肾动脉零应力状态的变化，并于SHR高血压形成前，分别给予口服型AugⅡⅠ型受体拮抗剂Losartan和ETA型受体拍抗剂BMS－182874，研究内源性AugⅡ和ET在SHR肾动脉零应力状态变化中的作用。结果发现，在高血压已建立的SHR，肾动脉主干的张开角（114．2±42．2度）显著大于同龄的WKY大鼠（70．2±30．4度）。给予SHRLosartan和BMS－182874（4～16周），SHR肾动脉主干的张开角均显著减小（分别为65．9±327度和66．6±41．54度）。结果表明，在已建立高血压的SHR，肾动脉主干存在非均匀生长，其残余应力、应变大于同龄的WKY，内源性AnsⅡ和ET在SHR肾动脉零应力状态的改变中起重要作用。
By observing the size of the opening angle of the renal artery, we investigated the change of zero-stress state of renal artery in spontaneously hypertensive rats (SHR) before and after the establishment of SHR. Before oral administration of Aug Ⅱ type I receptor Antagonist Losartan and ETA receptor antagonist BMS-182874 to study the role of endogenous Aug Ⅱ and ET in the changes of zero-stress state of SHR renal artery. The results showed that the open angle of the trunk of the renal artery (114.2 ± 42.2 degrees) was significantly greater than that of the WKY rats of the same age (70.2 ± 30.4 degrees) in SHR with established hypertension. SHRosartan and BMS-182874 (4 to 16 weeks) were significantly reduced in the open angle of the SHR renal arteries (65.9 ± 327 degrees and 66.6 ± 41.54 degrees, respectively). The results showed that there was non-uniform growth of renal artery in the established SHR, and its residual stress and strain were larger than WKY of the same age. Endogenous AnsⅡand ET played an important role in the change of zero-stress state of renal artery in SHR.