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"Step" vs. "dynamic" autoregulation: implications for susceptibility to hypertensive injury

Department of ¹Internal Medicine, Loyola University Medical Center and Edward Hines, Jr., Veterans Affairs Hospital, Maywood 60153; Department of ²Electrical and Computer Engineering, Illinois Institute of Technology, Chicago, Illinois 60616; and Department of ³Pharmacology and Therapeutics, University of Calgary, Alberta T2N 4N1, Canada

Submitted 13 January 2003 ; accepted in final form 5 March 2003

Renal autoregulatory (AR) mechanisms provide the primary protection against transmission of systemic pressures, and their impairment is believed to be responsible for the enhanced susceptibility to hypertensive renal damage in renal mass reduction (RMR) models. Assessment of AR capacity by the "step" change methodology under anesthesia was compared with that by "dynamic" methods in separate conscious control Sprague-Dawley rats and after uninephrectomy (UNX) and RMR (RK-NX) (n = 7–10/group). Substantially less AR capacity was seen by the dynamic vs. the step methodology in control rats. Moreover, dynamic AR capacity did not differ among controls, UNX, and RK-NX rats (fractional gain in admittance 0.4–0.5 in all groups at frequencies in the range of 0.0025–0.025 Hz). By contrast, significant impairment of step AR was seen in RK-NX vs. control or UNX rats (AR indexes 0.7 ± 0.1 vs. 0.1 ± 0.02 and 0.2 ± 0.04, respectively, P < 0.01). We propose that the step and dynamic methods evaluate the renal AR responses to different components of blood pressure (BP) power with the step AR assessing the ability to buffer large changes in average BP (DC power), whereas the present "dynamic" methods assess the AR ability to buffer slow BP fluctuations (<0.25 Hz) superimposed on the average BP (AC power), a substantially smaller component of total BP power. We further suggest that step but not dynamic AR methods as presently performed provide a valid index of the underlying susceptibility to hypertensive glomerular damage after RMR.

renal hemodynamics; hypertension; nephrosclerosis; myogenic response; tubuloglomerular feedback