Angiotensin II and the Renal Hemodynamic Response to an Isolated Increased Renal Venous Pressure in Rats

Figures

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  Figure 1. Changes in mean arterial pressure (MAP) and heart rate (HR) in response to increased renal venous pressure (RVP). The bar graphs show the baseline MAP (A) and HR (C) in untreated control (black, control, n=8), angiotensin II (ANG II) Clamp (grey, ANG II Clamp, n=10) and ANG II Absent (open bar, ANG II Absent, n=8, BP supported by AVP) rats. The line charts represent changes from baseline, △MAP (B), and △HR (D). In the line chart, the first two time points in each line represent baseline. The latter four time points show control (●, control) and major RVP elevation (△, RVP20). Baseline MAP did not differ among groups (A). Increased RVP caused a significant decrease in MAP in the ANG II Clamp group (B; *p<0.05) but not in untreated control group or ANG II Absent group. Baseline HR was significantly lower in the ANG II Absent group than in untreated control and ANG II Clamp groups (C; *p<0.05). Increased RVP induced HR reduction in untreated control group and ANG II Clamp group (*p<0.05) but not in the ANG II Absent group (D). #Data from these were published in Huang et al. (2018).

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  Figure 2. Changes in HR per changes in MAP in untreated rats and ANG II Clamp rats. The ratio of the change in heart rate vs. the change in MAP of the baseline measurements vs. the measurements at 90 and 120min was calculated for each animal. Groups, untreated Time Controls (TC, n=9), untreated animals subjected to increased RVP (n=8), ANG II Clamp time controls (not subjected to an increase in RVP, n=8), and ANG II Clamp animals subjected to increased RVP (n=10) were compared using two-way ANOVA with Bonferroni correction.

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  Figure 3. Changes in renal blood flow (RBF), renal vascular conductance (RVC), and glomerular filtration rate (GFR) in response to increased RVP. The bar graphs show the baseline RBF (A), RVC (B), and GFR (C) in untreated control (black, control, n=8), ANG II Clamp (gray, ANG II Clamp, n=10) and ANG II Absent (open bar, ANG II Absent, n=8, BP supported by AVP) rats. The line charts show changes from baseline, △RBF (B), △RVC (D), and △GFR (F). In the line chart, the first two time points in each line represent baseline. The latter four time points show control (●, control) and major RVP elevation (△, RVP20). Baseline RBF was significantly higher in the ANG II Absent group than in untreated control and ANG II Clamp group (A; *p<0.05). Elevation of RVP reduced RBF in untreated control group (B; **p<0.001), in ANG II Clamp and ANG II Absent groups (B; *p<0.05). Baseline RVC was higher in ANG II Absent group (C; *p<0.05). Increased RVP reduced RVC in untreated control group (D; *p<0.05), but did not impact RVC in either ANG II Clamp or ANG II Absent group. Baseline GFR was higher in the ANG II Absent group than in the other groups (E; *p<0.05). Increased RVP caused significant reduction of GFR…

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  Figure 4. Renal blood flow autoregulation curves. Each curve is generated by nonlinear regression analysis. (A,C,E) show baseline autoregulation curves before RVP manipulation. (B,D,F) show autoregulation curves without RVP elevation (B, TC, n=6), with RVP elevation of ~10mmHg (D, RVP 10, n=8) and with RVP elevation of ~20mmHg (F, RVP 20, n=8). The red curve indicates the average of the curves. The lower limit of RBF autoregulation is indicated by the vertical dashed line.

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  Figure 5. Passive pressure changes in vascular bed when RVP is increased. When pressure is increased in the venous system without neurohumoral adjustment, the glomerular capillary hydrostatic pressure is increased passively.