Renovascular adaptive changes in chronic hypoxic polycythemia

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Renovascular adaptive changes in chronic hypoxic polycythemia C. Dennis Thron, Jian Chen, James C. Leiter, Lo Chang Ou  Kidney International  Volume 54, Issue 6, Pages 2014-2020 (January 1998) DOI: 10.1046/j.1523-1755.1998.00186.x Copyright © 1998 International Society of Nephrology Terms and Conditions

Figure 1 Renal blood flow (A), renal plasma flow (B), filtration fraction (C) and glomerular filtration rate (D) have been plotted as functions of the hematocrit (Hct). Analysis of covariance showed no significant differences between the Madison (○) and Hilltop (•) rats, and the regression lines shown are for pooled data from both strains. Slopes and significance values are: renal blood flow, 91.2 ± 8.8 μl/min/100g body wt/% Hct, P < 0.001; renal plasma flow, -17.2 ± 4.3 μl/min/100g body wt/% Hct, P < 0.001; filtration fraction, 0.0036 ± 0.0010% filtration/% Hct, P < 0.002; glomerular filtration rate, -3.2 ± 2.2 μl/min/100g body wt/% Hct, P = 0.17. Kidney International 1998 54, 2014-2020DOI: (10.1046/j.1523-1755.1998.00186.x) Copyright © 1998 International Society of Nephrology Terms and Conditions

Figure 2 Calculated renal vascular resistance (A) and renal vascular hindrance (B) have been plotted as functions of the hematocrit. The renal vascular hindrance was calculated by dividing renal vascular resistance by viscosity in centipoises. Viscosity was estimated from the hematocrit-viscosity curve[15], assuming a shear rate of 200/sec. Comparisons between strains have not been calculated since renal vascular resistance and renal vascular hindrance are linearly dependent on arterial blood pressure and RBF, which did not differ between strains. The renal vascular hindrance data were fitted to a second order polynomial since the goodness of fit was superior to linear regression. Equations for the plotted curves: renal vascular resistance = 42.74-0.38 × Hct; renal vascular hindrance = 28.85-0.71 × Hct + 0.00465 × Hct2. Symbols are (○) Madison and (•) Hilltop rats. Kidney International 1998 54, 2014-2020DOI: (10.1046/j.1523-1755.1998.00186.x) Copyright © 1998 International Society of Nephrology Terms and Conditions

Figure 3 Renal oxygen delivery (A) and renal oxygen consumption (B) have been plotted as functions of the hematocrit. The triangles represent sea level, normoxic values, and the circles represent hypoxic values. (A) Regarding renal oxygen delivery, the regression slopes for hypoxic conditions (normoxic points excluded) differ significantly for the two strains (P < 0.05, analysis of covariance). Slopes and P values are: Madison, 1.59 ± 0.20ml/min/100g body wt/% Hct, P < 0.001; Hilltop, 1.17 ± 0.08ml/min/100g body wt/% Hct, P < 0.001. For renal oxygen consumption (B), the regression slopes did not differ significantly between rat strains (Hilltop, slope = 0.077 ± 0.028mol/min/100g body wt/% Hct, P < 0.02; Madison, slope = 0.071 ± 0.038mol/min/100g body wt/% Hct, P = 0.07). However, renal oxygen consumption was higher in Hilltop rats across all hematocrits compared to Madison rats (P = 0.01 for adjusted means, analysis of covariance). Kidney International 1998 54, 2014-2020DOI: (10.1046/j.1523-1755.1998.00186.x) Copyright © 1998 International Society of Nephrology Terms and Conditions