1. Volume 62, Issue 1, Pages 181-191 (July 2002)
Impaired coronary endothelial function in a rat model of spontaneous albuminuria 
Simone Gschwend, Sara-Joan Pinto-Sietsma, Hendrik Buikema, Yigal M. Pinto, Wiek H. Van Gilst, Angela Schulz, Dick De Zeeuw, Reinhold Kreutz 
Kidney International 
Volume 62, Issue 1, Pages (July 2002)
DOI: /j x
Copyright © 2002 International Society of Nephrology Terms and Conditions

2. Figure 1
Characteristics of Wistar (□,N = 10), MFW (■,N = 10), and SHR (▪,N = 9). (A) Systolic blood pressure (SBP), (B) heart weight to body weight ratio (HW/BW), and (C) urinary albumin excretion (UAE). Data are given as mean ± SEM; * and # indicate P < 0.05 vs. Wistar and MWF, respectively.
Kidney International  , DOI: ( /j x)
Copyright © 2002 International Society of Nephrology Terms and Conditions

3. Figure 2
Concentration-response curves to the endothelium-dependent dilator acetylcholine (ACh) in isolated arteries of Wistar (•,N = 10), MWF (▪,N = 10), and SHR (▴,N = 9). (A) Coronary arteries preconstricted with serotonin (*P < 0.05 vs. MWF for Emax). (B) Mesenteric arteries preconstricted with phenylephrine (* and # indicate P < 0.05 vs. SHR for Emax and pD2, respectively). Data are given as mean ± SEM.
Kidney International  , DOI: ( /j x)
Copyright © 2002 International Society of Nephrology Terms and Conditions

4. Figure 3
Concentration-response curves to the endothelium-independent dilator sodium nitrite (SN) in isolated arteries of Wistar (•,N = 10), MWF (▪,N = 10), and SHR (▴,N = 9). (A) Coronary arteries preconstricted with serotonin and (B) mesenteric arteries preconstricted with phenylephrine. Data are given as mean ± SEM; * and # indicate P < 0.05 vs. SHR for Emax and pD2 respectively.
Kidney International  , DOI: ( /j x)
Copyright © 2002 International Society of Nephrology Terms and Conditions

5. Figure 4
Effect of NO-blockade and additional prevention of endothelium-derived hyperpolarization (EDH) on acetylcholine (ACh)-induced relaxation in isolated coronary arteries of Wistar (A,N = 10), MWF (B,N = 10), and SHR (C,N = 9) rats. Responses were obtained in the continuous presence of 10-5 mol/L indomethacin (Control, •), either with or without additional presence of 10-4 mol/L L-NMMA only (▪), or 10-4 mol/L L-NMMA combined with 40 mmol/L KCl (▴). Data are given as mean ± SEM; * and # indicate P < 0.05 vs. control for Emax and pD2, respectively.
Kidney International  , DOI: ( /j x)
Copyright © 2002 International Society of Nephrology Terms and Conditions

6. Figure 5
Effect of NO-blockade and additional prevention of endothelium-derived hyperpolarization (EDH) on acetylcholine (ACh)-induced relaxation in isolated mesenteric arteries of Wistar (A,N = 10), MWF (B,N = 10), and SHR (C,N = 9) rats. Responses were obtained in the continuous presence of 10-5 mol/L indomethacin (Control, •), either with or without additional presence of 10-4 mol/L L-NMMA only (▪), or 10-4 mol/L L-NMMA combined with 40 mmol/L KCl (▴). Data are given as mean ± SEM; * and # indicate P < 0.05 vs. control for Emax and pD2, respectively.
Kidney International  , DOI: ( /j x)
Copyright © 2002 International Society of Nephrology Terms and Conditions

7. Figure 6
Overview of NO and EDH contribution to acetylcholine (ACh)-induced relaxation in (A) coronary arteries and (B) mesenteric arteries of Wistar (□,N = 10), MWF (■,N = 10) and SHR (▪,N = 9) rats. The area under the concentration response curve (AUC, arbitrary units) to ACh was used to represent total response-size. NO and EDH contribution were then calculated as those parts of the response to ACh that were sensitive to inhibition with 10-4 mol/L L-NMMA and 40 mmol/L KCl, respectively (Methods section). Data are given as mean ± SEM; *P < 0.05 vs. Wistar, and #P < 0.05 vs. MWF.
Kidney International  , DOI: ( /j x)
Copyright © 2002 International Society of Nephrology Terms and Conditions