Quirk W S, Wright J W, Dengerink H A, Miller J M
Department of Psychology, Washington State University, Pullman 99164-4830.
Hear Res. 1988 May;33(2):129-35. doi: 10.1016/0378-5955(88)90025-1.
Previous investigations in our laboratory have measured significant increases in the circulating levels of the potent vasoconstrictive hormone, angiotensin II (AII; 26 and 64 pg/100 microliters plasma, normal and noise exposed, respectively), during and following noise exposure in the alert rat (Wright et al., 1981). In the present study, these levels were approximated through intra-arterial infusion in the anesthetized spontaneously hypertensive rat (SHR) and normotensive Wistar-Kyoto (WKY) rat. Laser Doppler flowmeter measurements of cochlear blood flow (CBF) indicated that despite equivalent AII-induced elevations in systemic blood pressure, CBF in the SHR did not increase to the levels measured in the WKY. Pretreatment with the specific angiotensin receptor antagonist sarile, (Sar1,Ile8-AII), reduced AII-induced elevations in systemic blood pressure in members of both strains, but did not change the overall pattern of CBF. These results indicate that SHRs may have a compromised cochlear circulation that is refractory to increases in systemic blood pressure.
我们实验室之前的研究已经测量到，在警觉大鼠暴露于噪声期间及之后，强效血管收缩激素血管紧张素II（AII；正常大鼠和噪声暴露大鼠的血浆水平分别为26和64 pg/100微升）的循环水平显著升高（Wright等人，1981年）。在本研究中，通过对麻醉的自发性高血压大鼠（SHR）和正常血压的Wistar-Kyoto（WKY）大鼠进行动脉内输注来近似这些水平。激光多普勒血流仪测量耳蜗血流量（CBF）表明，尽管AII引起的全身血压升高程度相同，但SHR中的CBF并未升高到WKY中测量的水平。用特异性血管紧张素受体拮抗剂sarile（Sar1，Ile8-AII）进行预处理，可降低两种品系大鼠中AII引起的全身血压升高，但并未改变CBF的总体模式。这些结果表明，SHR的耳蜗循环可能受损，对全身血压升高具有抗性。
