Autoregulation of cochlear blood flow in normotensive and spontaneously hypertensive rats following intracerebroventricularly mediated adjustment of blood pressure.

Previous studies in our laboratory (Quirk et al., 1988) noted significantly impaired elevations in cochlear blood flow (CoBF) during systemic infusion of the potent vasoconstrictive agent angiotensin II (AII) in the spontaneously hypertensive rat (SHR) as compared with the normotensive Wistar-Kyoto (WKY) rat, despite similar increases in systemic blood pressure. We interpreted these results to suggest that SHRs have an exaggerated autoregulatory mechanism that controls blood supply to the cochlear vessels. However, an alternative explanation for these findings concerns the potential influence of the elevated baseline blood pressure of the SHR on CoBF. Specifically, if there is an absolute threshold blood pressure that triggers an autoregulatory response in the cochlea, then the SHRs would reach that threshold sooner than normotensive animals because they begin at a baseline blood pressure that is well above that of the WKY rat. The present study addressed this possibility by pharmacologically reducing SHR blood pressure to WKY baseline blood pressure and raising WKY to SHR baselines, followed by the infusion of previously utilized doses of AII. The results are consistent with previous findings and support our interpretation of an exaggerated autoregulation of cochlear blood supplying the SHR.