Attenuated buffering of renal perfusion pressure variation in juxtamedullary cortex in SHR.

Renal tissue damage is substantially more pronounced in the juxtamedullary than in the superficial cortex in hypertensive rats, and the pathogenesis of the morphological changes are only partly understood. Glomerular capillary pressure (P(GC)) is increased, and steady-state autoregulation is normal in the deep renal cortex. We tested the hypothesis that the transient period from one pressure level to another may induce greater variation in local perfusion before stable autoregulation is established. An acute increase in local perfusion was compared in the superficial and juxtamedullary cortex of spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY) after an abrupt increase in perfusion pressure. Total renal blood flow (RBF) was measured by a Transonic flow probe and local renal perfusion by laser Doppler flowmetry. Renal perfusion pressure was lowered to 50% of initial values and released abruptly. The maximal RBF increased from 6.3 +/- 0.4 to a maximal value of 7.6 +/- 0.3 ml/min (P < 0.001) in SHR and from 7.3 +/- 0.3 to 8.2 +/- 0.6 ml/min (P < 0.001) in WKY. These changes were not significantly different from each other. The change in superficial cortical perfusion was also not different between SHR and WKY. Pressure release increased juxtamedullary perfusion in SHR from 146 +/- 8 to a maximal value of 228 +/- 17 units (P < 0.001) and in WKY from 160 +/- 13 to 179 +/- 11 units (P < 0.001). The results were significantly different from each other (P < 0.001). The time for maximal flow response was shorter in the deep cortex of SHR, and the time for normalization was longer than in WKY. These data indicate that the buffering of perfusion pressure variation is significantly attenuated in the juxtamedullary cortex, and significantly more so in SHR than in WKY, assuming a covariation of RBF and P(GC), and this finding may explain the extensive morphological damage in the juxtamedullary cortex of SHR.