RESETTING OF RENAL BLOOD AUTOREGULATION DURING ACUTE BLOOD-PRESSURE REDUCTION IN HYPERTENSIVE RATS

Decrease in systemic blood pressure, duration of pressure decrease, an d change in the activity of the renin or the sympathetic nervous syste m may represent mechanisms involved in resetting the renal blood flow (RBF) autoregulation found in hypertensive rats. Autoregulation of RBF , plasma renin concentration (PRC), and the time needed for resetting to take place were studied in the nonclipped kidney before and after r emoval of the clipped kidney of two-kidney, one-clip (2K1C) hypertensi ve rats and before and after mechanical reduction of the renal arteria l pressure (R4P) for 10 min in the spontaneously hypertensive rat (SHR ) and in the nonclipped kidney of 2K1C hypertensive rats with and with out renal denervation. Mean arterial pressure (MAP) fell from 147 to 1 07 mmHg 30 min after removal of the clipped kidney, and the lower pres sure limit of RBF autoregulation decreased from 113 to 90 mmHg (P < 0. 01); PRC fell. Mechanical reductions of RAP from 161 to 120 mmHg in th e nonclipped kidney for 10 min did not change RBF, but at 120 mmHg, th e lower pressure limit of RBF autoregulation was reduced from 115 mmHg before pressure reduction to 96 mmHg afterwards (P < 0.02). In SHR, s imilar pressure reduction for 10 min decreased the lower pressure limi t of RBF autoregulation from 106 to 86 mmHg (P < 0.01). PRC was unchan ged in both models, and denervation did not change RBF autoregulation. When RAP was reduced below the lower pressure limit of RBF autoregula tion, RBF decreased similar to 20%; the lower pressure limit of RBF au toregulation remained unchanged. In normotensive Wistar-Kyoto rats, pr essure reduction did not change the range of RBF autoregulation. These results indicate that acute normalization of the pressure range of RB F autoregulation in hypertensive rats is dependent on the degree of pr essure reduction of RAP, whereas renal innervation and PRC do not play a major role. We propose that the mechanism of resetting is due to af terstretch of noncontractile elements of the vessel wall or is caused by pure myogenic mechanisms. An effect of intrarenal angiotensin canno t be excluded.