Association of a Disrupted Dipping Pattern of Blood Pressure with Progression of Renal Injury during the Development of Salt-Dependent Hypertension in Rats

Figures

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  Figure 1. Time-dependent changes of blood pressure and heart rate. Averaged 20-h (A) mean arterial pressure (MAP), (B) systolic blood pressure (SBP), (C) diastolic blood pressure (DBP), and (D) heart rate (HR) during feeding normal salt diet (NSD, 0.3% NaCl, week 7), high salt diet (HSD, 8% NaCl, weeks 8–17), and again after switching to NSD (week 18–21) in Dahl salt-sensitive (DSS) rats. * p < 0.05 vs. DSS rats with NSD; # p < 0.05, DSS rats with NSD→HSD→NSD (week 17) vs. DSS rats with NSD→HSD→NSD (week 18–21).

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  Figure 2. Circadian rhythm of MAP at baseline during feeding normal salt diet (NSD, 0.3% NaCl diet at week 7). (A) Hourly MAP with NSD, (B) averaged 10-h MAP in active and inactive periods, and (C) the difference of 10-h MAP between active and inactive periods. † p < 0.05, DSS rats with NSD→HSD→NSD (inactive period) vs. DSS rats with NSD→HSD→NSD (active period); ‡ p < 0.05; DSS rats with NSD (inactive period) vs. DSS rats with NSD (active period).

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  Figure 3. Circadian rhythm of MAP during feeding HSD (week 8–17). (A) Hourly MAP, (B) averaged 10-h MAP in active and inactive periods, and (C) the difference of 10-h MAP between active and inactive periods after 5 days of HSD. (D) Hourly MAP, (E) averaged 10-h MAP in active and inactive periods, and (F) the difference of 10-h MAP between active and inactive periods after 3 weeks of HSD. (G) Hourly MAP, (H) averaged 10-h MAP in active and inactive periods, and (I) the difference of 10-h MAP between active and inactive periods after 7 weeks of HSD. (J) Hourly MAP, (K) averaged 10-h MAP in active and inactive periods, and (L) the difference of 10-h MAP between active and inactive periods after 10 weeks of HSD in DSS rats. * p < 0.05 vs. DSS rats with NSD; † p < 0.05, DSS rats with NSD→HSD→NSD (inactive period) vs. DSS rats with NSD→HSD→NSD (active period); ‡ p < 0.05, DSS rats with NSD (inactive period) vs. DSS rats with NSD (active period).

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  Figure 4. Circadian rhythm of MAP after switching to NSD (week 18–21). (A) Hourly MAP, (B) averaged 10-h MAP in active and inactive periods, and (C) the difference of 10-h MAP between active and inactive periods at 4 weeks after switching HSD to NSD. * p < 0.05 vs. DSS rats with NSD; † p < 0.05, DSS rats with NSD→HSD→NSD (inactive period) vs. DSS rats with NSD→HSD→NSD (active period); ‡ p < 0.05, DSS rats with NSD (inactive period) vs. DSS rats with NSD (active period).

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  Figure 5. Effects of HSD on urinary protein excretion. (A) The 24-h urinary protein excretion, and (B) the urinary protein and creatinine (UproteinV/Ucr.V) ratio. (C) Correlation between differences in active and inactive period MAP and level of urinary protein excretion. (D) Correlation between differences in active and inactive period MAP and urinary protein–creatinine ratio. * p < 0.05 vs. DSS rats with NSD; # p < 0.05, DSS rats with NSD→HSD→NSD (week 17) vs. DSS rats with NSD→HSD→NSD (week 18–21).

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  Figure 6. Effects of HSD on renal glomerular and tubulointerstitial injury. (A) Representative’s images of PAS-stained renal sections (magnification, ×200; scale bar 50 μm). (B) The PAS-positive area within the glomerular area. (C) Representative micrographs of Azan-stained renal sections (magnification, ×100, scale bar 100 μm). (D) Quantitative analysis of Azan-positive area. * p < 0.05 vs. DSS rats with NSD.