Differential effects of salt on renal hemodynamics and potential pressure transmission in stroke-prone and stroke-resistant spontaneously hypertensive rats

Abstract

Salt-supplemented stroke-prone spontaneously hypertensive rats (SHRsp) develop more severe hypertension-induced renal damage (HIRD) compared with their progenitor SHR. The present studies were performed to examine whether in addition to increasing the severity of hypertension salt also enhanced the transmission of such hypertension to the renal vascular bed in the SHRsp. “Step” and “dynamic” renal blood flow (RBF) autoregulation (AR) were examined in ∼12-wk-old SHR and SHRsp after 3–5 days of an 8% NaCl diet. During step AR under anesthesia ( n = 8–11), RBF was significantly higher in the SHRsp at all perfusion pressures ( P < 0.01), but AR capacity was not different. Similarly, in separate conscious chronically instrumented rats ( n = 8 each), both blood pressure (BP) and RBF were modestly but significantly higher at baseline before salt in the SHRsp ( P < 0.05). However, transfer function analysis did not show significant differences in the admittance gain parameters. However, after 3–5 days of salt, although average BP was not significantly altered in either strain, RBF increased further in the SHRsp and there was a significantly greater transfer of BP into RBF power in the SHRsp. This was reflected in the significantly higher admittance gain parameters at most frequencies including the heartbeat frequency ( P < 0.05 maximum). These differential hemodynamic effects of salt have the potential to enhance BP transmission to the renal vascular bed and also contribute to the more severe HIRD observed in the salt-supplemented SHRsp.