Synergistic QTL interactions between Rf-1 and Rf-3 increase renal damage susceptibility in double congenic rats

The FHH (fawn-hooded hypertensive) rat is a model of hypertension-associated chronic kidney damage. Five interacting quantitative trait loci (QTLs), named Rf-1–Rf-5, determine the high renal susceptibility. The aim of the present study was to investigate a possible interaction between Rf-1 and Rf-3....

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Published in:	Kidney international Vol. 69; no. 8; pp. 1369 - 1376
Main Authors:	Van Dijk, S.J., Specht, P.A.C., Lazar, J., Jacob, H.J., Provoost, A.P.
Format:	Journal Article
Language:	English
Published:	New York, NY Elsevier Inc 01.04.2006 Nature Publishing Elsevier Limited
Subjects:	Administration, Oral Animals Animals, Congenic Biological and medical sciences Blood Pressure - genetics Chromosome Mapping Chromosomes, Mammalian congenic rats Enzyme Inhibitors - administration & dosage Follow-Up Studies Genetic Markers Genetic Predisposition to Disease Genome Homeostasis - genetics Homozygote Hypertension, Renal - etiology Hypertension, Renal - genetics Kidney Diseases - genetics Kidney Diseases - physiopathology L-NAME-hypertension Male Medical sciences Nephrectomy Nephrology. Urinary tract diseases NG-Nitroarginine Methyl Ester - administration & dosage proteinuria Proteinuria - genetics Quantitative Trait Loci Rats Rats, Inbred ACI Renal Circulation - genetics renal damage susceptibility Survival Analysis Time Factors unilateral nephrectomy Urinary system involvement in other diseases. Miscellaneous Urinary tract. Prostate gland renal damage susceptibility L-NAME-hypertension congenic rats unilateral nephrectomy proteinuria Nephrology Rat Quantitative character Cardiovascular disease Synergism Kidney Urology Nephrectomy Surgery Congenic Drug interaction Hypertension Urinary system disease Rodentia Vertebrata Mammalia Treatment Urinary system Animal Unilateral Lesion Proteinuria
ISSN:	0085-2538, 1523-1755
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Abstract	The FHH (fawn-hooded hypertensive) rat is a model of hypertension-associated chronic kidney damage. Five interacting quantitative trait loci (QTLs), named Rf-1–Rf-5, determine the high renal susceptibility. The aim of the present study was to investigate a possible interaction between Rf-1 and Rf-3. Differences in renal susceptibility between ACI (August × Copenhagen Irish) controls, Rf-1A and Rf-3 single congenics, and Rf-1A+3 double congenic rats were assessed using four different treatments: two-kidney control (2K), 2K plus Nω-nitro-L-arginine methyl ester (L-NAME)-induced hypertension (2K+L-NAME), unilateral nephrectomy (UNX), and UNX plus L-NAME-induced hypertension (UNX+L-NAME). Proteinuria (UPV) and systolic blood pressure (SBP) were assessed after 6, 12, and 18 weeks, while the incidence of glomerulosclerosis (%FGS) was determined at the end of the experiment. In a separate experiment, renal autoregulation was assessed in 13–15-week old 2K rats of all four strains. Compared to ACI rats, small increases in renal susceptibility were found in Rf-1A and Rf-3 single congenics following 2K+L-NAME, UNX, and UNX+L-NAME treatments. However, in the Rf-1A+3 double congenics, a major increase in renal susceptibility was found with all four treatments. Both Rf-1A and Rf-1A+3 congenic rats had an impaired renal autoregulation. In contrast, the Rf-3 had a normal autoregulation, similar to that of the ACI rat. These findings indicate that Rf-1 and Rf-3 alone slightly increase the susceptibility to the development of renal damage. However, a synergistic interaction between these two QTLs markedly enhances renal susceptibility. In contrast to the Rf-1 region, the Rf-3 region does not carry genes influencing renal autoregulation.
AbstractList	The FHH (fawn-hooded hypertensive) rat is a model of hypertension-associated chronic kidney damage. Five interacting quantitative trait loci (QTLs), named Rf-1-Rf-5, determine the high renal susceptibility. The aim of the present study was to investigate a possible interaction between Rf-1 and Rf-3. Differences in renal susceptibility between ACI (August x Copenhagen Irish) controls, Rf-1A and Rf-3 single congenics, and Rf-1A+3 double congenic rats were assessed using four different treatments: two-kidney control (2K), 2K plus N(omega)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension (2K+L-NAME), unilateral nephrectomy (UNX), and UNX plus L-NAME-induced hypertension (UNX+L-NAME). Proteinuria (UPV) and systolic blood pressure (SBP) were assessed after 6, 12, and 18 weeks, while the incidence of glomerulosclerosis (%FGS) was determined at the end of the experiment. In a separate experiment, renal autoregulation was assessed in 13-15-week old 2K rats of all four strains. Compared to ACI rats, small increases in renal susceptibility were found in Rf-1A and Rf-3 single congenics following 2K+L-NAME, UNX, and UNX+L-NAME treatments. However, in the Rf-1A+3 double congenics, a major increase in renal susceptibility was found with all four treatments. Both Rf-1A and Rf-1A+3 congenic rats had an impaired renal autoregulation. In contrast, the Rf-3 had a normal autoregulation, similar to that of the ACI rat. These findings indicate that Rf-1 and Rf-3 alone slightly increase the susceptibility to the development of renal damage. However, a synergistic interaction between these two QTLs markedly enhances renal susceptibility. In contrast to the Rf-1 region, the Rf-3 region does not carry genes influencing renal autoregulation. The FHH (fawn-hooded hypertensive) rat is a model of hypertension-associated chronic kidney damage. Five interacting quantitative trait loci (QTLs), named Rf-1–Rf-5, determine the high renal susceptibility. The aim of the present study was to investigate a possible interaction between Rf-1 and Rf-3. Differences in renal susceptibility between ACI (August × Copenhagen Irish) controls, Rf-1A and Rf-3 single congenics, and Rf-1A+3 double congenic rats were assessed using four different treatments: two-kidney control (2K), 2K plus Nω-nitro-L-arginine methyl ester (L-NAME)-induced hypertension (2K+L-NAME), unilateral nephrectomy (UNX), and UNX plus L-NAME-induced hypertension (UNX+L-NAME). Proteinuria (UPV) and systolic blood pressure (SBP) were assessed after 6, 12, and 18 weeks, while the incidence of glomerulosclerosis (%FGS) was determined at the end of the experiment. In a separate experiment, renal autoregulation was assessed in 13–15-week old 2K rats of all four strains. Compared to ACI rats, small increases in renal susceptibility were found in Rf-1A and Rf-3 single congenics following 2K+L-NAME, UNX, and UNX+L-NAME treatments. However, in the Rf-1A+3 double congenics, a major increase in renal susceptibility was found with all four treatments. Both Rf-1A and Rf-1A+3 congenic rats had an impaired renal autoregulation. In contrast, the Rf-3 had a normal autoregulation, similar to that of the ACI rat. These findings indicate that Rf-1 and Rf-3 alone slightly increase the susceptibility to the development of renal damage. However, a synergistic interaction between these two QTLs markedly enhances renal susceptibility. In contrast to the Rf-1 region, the Rf-3 region does not carry genes influencing renal autoregulation. The FHH (fawn-hooded hypertensive) rat is a model of hypertension-associated chronic kidney damage. Five interacting quantitative trait loci (QTLs), named Rf-1-Rf-5, determine the high renal susceptibility. The aim of the present study was to investigate a possible interaction between Rf-1 and Rf-3. Differences in renal susceptibility between ACI (August x Copenhagen Irish) controls, Rf-1A and Rf-3 single congenics, and Rf-1A+3 double congenic rats were assessed using four different treatments: two-kidney control (2K), 2K plus N(omega)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension (2K+L-NAME), unilateral nephrectomy (UNX), and UNX plus L-NAME-induced hypertension (UNX+L-NAME). Proteinuria (UPV) and systolic blood pressure (SBP) were assessed after 6, 12, and 18 weeks, while the incidence of glomerulosclerosis (%FGS) was determined at the end of the experiment. In a separate experiment, renal autoregulation was assessed in 13-15-week old 2K rats of all four strains. Compared to ACI rats, small increases in renal susceptibility were found in Rf-1A and Rf-3 single congenics following 2K+L-NAME, UNX, and UNX+L-NAME treatments. However, in the Rf-1A+3 double congenics, a major increase in renal susceptibility was found with all four treatments. Both Rf-1A and Rf-1A+3 congenic rats had an impaired renal autoregulation. In contrast, the Rf-3 had a normal autoregulation, similar to that of the ACI rat. These findings indicate that Rf-1 and Rf-3 alone slightly increase the susceptibility to the development of renal damage. However, a synergistic interaction between these two QTLs markedly enhances renal susceptibility. In contrast to the Rf-1 region, the Rf-3 region does not carry genes influencing renal autoregulation.The FHH (fawn-hooded hypertensive) rat is a model of hypertension-associated chronic kidney damage. Five interacting quantitative trait loci (QTLs), named Rf-1-Rf-5, determine the high renal susceptibility. The aim of the present study was to investigate a possible interaction between Rf-1 and Rf-3. Differences in renal susceptibility between ACI (August x Copenhagen Irish) controls, Rf-1A and Rf-3 single congenics, and Rf-1A+3 double congenic rats were assessed using four different treatments: two-kidney control (2K), 2K plus N(omega)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension (2K+L-NAME), unilateral nephrectomy (UNX), and UNX plus L-NAME-induced hypertension (UNX+L-NAME). Proteinuria (UPV) and systolic blood pressure (SBP) were assessed after 6, 12, and 18 weeks, while the incidence of glomerulosclerosis (%FGS) was determined at the end of the experiment. In a separate experiment, renal autoregulation was assessed in 13-15-week old 2K rats of all four strains. Compared to ACI rats, small increases in renal susceptibility were found in Rf-1A and Rf-3 single congenics following 2K+L-NAME, UNX, and UNX+L-NAME treatments. However, in the Rf-1A+3 double congenics, a major increase in renal susceptibility was found with all four treatments. Both Rf-1A and Rf-1A+3 congenic rats had an impaired renal autoregulation. In contrast, the Rf-3 had a normal autoregulation, similar to that of the ACI rat. These findings indicate that Rf-1 and Rf-3 alone slightly increase the susceptibility to the development of renal damage. However, a synergistic interaction between these two QTLs markedly enhances renal susceptibility. In contrast to the Rf-1 region, the Rf-3 region does not carry genes influencing renal autoregulation.
Author	Jacob, H.J. Specht, P.A.C. Lazar, J. Van Dijk, S.J. Provoost, A.P.
Author_xml	– sequence: 1 givenname: S.J. surname: Van Dijk fullname: Van Dijk, S.J. organization: Department of Pediatric Surgery, Erasmus MC, Rotterdam, The Netherlands – sequence: 2 givenname: P.A.C. surname: Specht fullname: Specht, P.A.C. organization: Department of Pediatric Surgery, Erasmus MC, Rotterdam, The Netherlands – sequence: 3 givenname: J. surname: Lazar fullname: Lazar, J. organization: Department of Dermatology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA – sequence: 4 givenname: H.J. surname: Jacob fullname: Jacob, H.J. organization: Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA – sequence: 5 givenname: A.P. surname: Provoost fullname: Provoost, A.P. email: a.provoost@erasmusmc.nl organization: Department of Pediatric Surgery, Erasmus MC, Rotterdam, The Netherlands
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Keywords	renal damage susceptibility L-NAME-hypertension congenic rats unilateral nephrectomy proteinuria Nephrology Rat Quantitative character Cardiovascular disease Synergism Kidney Urology Nephrectomy Surgery Congenic Drug interaction Hypertension Urinary system disease Rodentia Vertebrata Mammalia Treatment Urinary system Animal Unilateral Lesion Proteinuria
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Snippet	The FHH (fawn-hooded hypertensive) rat is a model of hypertension-associated chronic kidney damage. Five interacting quantitative trait loci (QTLs), named...
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SubjectTerms	Administration, Oral Animals Animals, Congenic Biological and medical sciences Blood Pressure - genetics Chromosome Mapping Chromosomes, Mammalian congenic rats Enzyme Inhibitors - administration & dosage Follow-Up Studies Genetic Markers Genetic Predisposition to Disease Genome Homeostasis - genetics Homozygote Hypertension, Renal - etiology Hypertension, Renal - genetics Kidney Diseases - genetics Kidney Diseases - physiopathology L-NAME-hypertension Male Medical sciences Nephrectomy Nephrology. Urinary tract diseases NG-Nitroarginine Methyl Ester - administration & dosage proteinuria Proteinuria - genetics Quantitative Trait Loci Rats Rats, Inbred ACI Renal Circulation - genetics renal damage susceptibility Survival Analysis Time Factors unilateral nephrectomy Urinary system involvement in other diseases. Miscellaneous Urinary tract. Prostate gland
Title	Synergistic QTL interactions between Rf-1 and Rf-3 increase renal damage susceptibility in double congenic rats
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