A High Salt Diet Does Not Alter the Kinetics or the Magnitude of Renal Blood Flow Autoregulation in Conscious Salt‐Resistant and Salt‐Sensitive Rats
Authors: Polichnowski Aaron J. , Griffin Karen A. , Williamson Geoffrey A. , Bidani Anil K. 
Published: May 2022

Blood pressure (BP) salt‐sensitivity is a major public health problem that augments the risk of kidney disease. Both BP dependent and independent mechanisms are thought to contribute to the increased risk of kidney injury in salt‐sensitive (SS) populations. Previous studies have reported that high dietary salt intake impairs renal blood flow (RBF) autoregulation, which increases the susceptibility to hypertensive renal injury. However, in these studies, RBF autoregulation was assessed in anesthetized rats or in isolated renal resistance vessels, which do not fully characterize the dynamic nature of RBF autoregulation in the conscious state. Our group has recently developed novel analytical methods to characterize both the magnitude and kinetics of the RBF autoregulatory response to spontaneous BP fluctuations in conscious, chronically instrumented rats. The goal of this study was to assess the effects of a high salt diet on the dynamics of RBF autoregulation in conscious, salt‐resistant and SS rat strains. At 8‐13 weeks of age, male Sprague‐Dawley (SD), Dahl SS, Consomic SS.BN1, Spontaneously Hypertensive (SHR), and Stroke‐prone SHR (SHRsp) rats were instrumented with a BP radiotelemeter and an ultrasonic RBF probe was positioned on the left renal artery. Following 1 week of recovery, BP and RBF were assessed for 2‐3 hours/day over 2‐3 consecutive days while rats were maintained on normal salt diet (0.4‐1% NaCl). All rats were then administered a high salt diet (4‐8% NaCl) and 2‐3 days later, BP and RBF were assessed for 2‐3 hours/day over 3‐5 consecutive days. All recordings were divided into segments of varying length (0.5‐20 seconds), and adjacent segments which exhibited a BP difference of 5 mmHg or greater were used to calculate RBF autoregulatory indices (i.e., % change in RBF / % change in BP). Different segment lengths were used to infer the time required for the preglomerular vasculature to restore RBF to levels observed prior to the change in BP. As shown in Figure 1, BP was significantly different among strains during normal salt diet with SD < SS.BN1 < SS = SHR < SHRsp. A high salt diet significantly increased BP in SS and SHR rats. No significant differences in RBF were found among all strains during normal or high salt intake, and a high salt diet did not significantly alter the RBF autoregulatory response in any strain (Figure 2). As also shown in Figure 2, all strains exhibited > 60% RBF autoregulatory compensation by 2.5 seconds following a change in BP, and the response was significantly faster in SHRsp vs. SD, SS, and SS.BN1 strains. All strains except SS and SS.BN1 rats exhibited complete RBF compensation by 10‐20 seconds following a change in BP. We conclude that a high salt diet does not significantly alter RBF autoregulatory responses in the conscious state in the salt‐resistant or salt‐sensitive strains examined in this study. There are strain differences in the initial magnitude of the RBF autoregulatory response with those strains exhibiting higher ambient BP’s having a stronger RBF autoregulatory response. The implications of the weaker RBF autoregulatory responses at later time points (i.e., 10‐20 seconds) following a change in BP in SS and SS.BN1 rats requires further investigation.