Analysis of renal autoregulation dynamics using linear fixed pole approach [Dogrusal sabit kutup yaklaşimi kullanarak böbrek otoregülasyonu dinamigi analizi]

IEEE 13th Signal Processing and Communications Applications Conference, SIU 2005 -- 16 May 2005 through 18 May 2005 -- Kayseri -- 69003The dynamics of renal autoregulation are modeled using linear nonparametric and parametric techniques. The Fixed Pole approach has been proposed and a data-dependent procedure is used for selecting the pole locations. This approach is applied the modeling technique to renal blood pressure and renal blood flow measurements in conscious rats. The pole location shows a quantitative characterization of frequency dependent features of the renal autoregulatory response which myogenic and TGF mechanisms are responsible for. The model is used to characterize the myogenic and TGF autoregulatory response in control rats and rats whose renal autoregulation has been impaired by calcium channel blockers. © 2005 IEEE

Spontaneously reduced blood pressure load in the rat streptozotocin-induced diabetes model: Potential pathogenetic relevance

The rat streptozotocin (STZ)-induced diabetes model is widely used to investigate the pathogenesis of diabetic nephropathy. However, overt nephropathy is inexplicably slow to develop in this model compared with renal mass reduction (RMR) models. To examine whether blood pressure (BP) differences correlated with the time course of glomerulosclerosis (GS), BP was measured continuously throughout the course by radiotelemetry in control (n = 17), partially insulin-treated STZ-diabetes (average blood glucose 364 ± 15 mg/dl; n = 15), and two normotensive RMR models (systolic BP <140 mmHg) - uninephrectomy (UNX; n = 16) and 3/4 RMR by surgical excision [right nephrectomy + excision of both poles of left kidney (RK-NX); n = 12] in Sprague-Dawley rats. Proteinuria and GS were assessed at ~16-20 wk (all groups) and at 36-40 wk (all groups except RK-NX). At 16 wk, significantly greater proteinuria and GS had developed in the RK-NX group compared with the other three groups (not different from each other). By 36-40 wk, substantial proteinuria and GS had also developed in the UNX group, but both the control and the STZ-diabetic rats exhibited comparable modest proteinuria and minimal GS. Systolic BP (mmHg) was significantly reduced in the STZ-diabetic rats (116 ± 1.1) compared with both control (124 ± 1.0) and RMR (128 ± 1.2 and 130 ± 3.0) groups (P < 0.01). Similarly, "BP load" as estimated by BP power spectral analysis was also lower in the STZ-diabetic rats. Given the known protective effects of BP reductions on the progression of diabetic nephropathy, it is likely that this spontaneous reduction in ambient BP contributes to the slow development of GS in the STZ-diabetes model compared with the normotensive RMR models

Characterization of dynamics in renal autoregulation using Volterra models

The dynamics of renal autoregulation are modeled using a modified Volterra representation called the fixed pole expansion technique (FPET). A data dependent procedure is proposed for selecting the pole locations in this expansion that enables a reduction in model complexity compared to standard Volterra models. Furthermore, a quantitative characterization of frequency dependent features of the renal autoregulatory response is enabled via the model's pole locations. The utility of this approach is demonstrated by applying the modeling technique to renal blood pressure and renal blood flow measurements in conscious rats. The model is used to characterize the myogenic autoregulatory response in control rats and rats whose renal autoregulation has been impaired by calcium channel blockers. © 2006 IEEE.Office of Academic Affiliations, Department of Veterans Affairs National Institute of Diabetes and Digestive and Kidney Diseases: DK-40426, DK-61653Manuscript received September 17, 2004; revised April 30, 2006. This work was supported in part by National Institutes of Diabetes and Digestive and Kidney Diseases under Grant DK-40426 and Grant DK-61653 and in part by the Office of Research and Development of the Department of Veterans Affairs. Asterisk indicates corresponding author. *R. Hacıog^lu was with the Department of Electrical and Computer Engineering, Illinois Institute of Technology Chicago, IL 60616 USA. He is now with the Department of Electrical and Electronics Engineering, Zonguldak Karaelmas University, Zonguldak 67100, Turkey (e-mail: [email protected])

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

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