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Allen W Cowley - One of the best experts on this subject based on the ideXlab platform.
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narrowing a region on rat Chromosome 13 that protects against hypertension in dahl ss 13bn congenic strains
American Journal of Physiology-heart and Circulatory Physiology, 2011Co-Authors: Carol Moreno, Howard J Jacob, Jan M Williams, Mingyu Liang, Jozef Lazar, Limin Lu, Allen W CowleyAbstract:Transfer of Chromosome 13 from the Brown Norway (BN) rat onto the Dahl salt-sensitive (SS) genetic background attenuates the development of hypertension, but the genes involved remain to be identified. The purpose of the present study was to confirm by telemetry that a congenic strain [SS.BN-(D13Hmgc37-D13Got22)/Mcwi, line 5], carrying a 13.4-Mb segment of BN Chromosome 13 from position 32.4 to 45.8 Mb, is protected from the development of hypertension and then to narrow the region of interest by creating and phenotyping 11 additional subcongenic strains. Mean arterial pressure (MAP) rose from 118 ± 1 to 186 ± 5 mmHg in SS rats fed a high-salt diet (8.0% NaCl) for 3 wk. Protein excretion increased from 56 ± 11 to 365 ± 37 mg/day. In contrast, MAP only increased to 152 ± 9 mmHg in the line 5 congenic strain. Six subcongenic strains carrying segments of BN Chromosome 13 from 32.4 and 38.2 Mb and from 39.9 to 45.8 Mb were not protected from the development of hypertension. In contrast, MAP was reduced by ∼30 mmHg in five strains, carrying a 1.9-Mb common segment of BN Chromosome 13 from 38.5 to 40.4 Mb. Proteinuria was reduced by ∼50% in these strains. Sequencing studies did not identify any nonsynonymous single nucleotide polymorphisms in the coding region of the genes in this region. RT-PCR studies indicated that 4 of the 13 genes in this region were differentially expressed in the kidney of two subcongenic strains that were partially protected from hypertension vs. those that were not. These results narrow the region of interest on Chromosome 13 from 13.4 Mb (159 genes) to a 1.9-Mb segment containing only 13 genes, of which 4 are differentially expressed in strains partially protected from the development of hypertension.
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multiple blood pressure loci on rat Chromosome 13 attenuate development of hypertension in the dahl s hypertensive rat
Physiological Genomics, 2007Co-Authors: Carol Moreno, Howard J Jacob, Jozef Lazar, Mary L Kaldunski, Tao Wang, Richard J Roman, Andrew S Greene, Allen W CowleyAbstract:Previous studies have indicated that substitution of Chromosome 13 of the salt-resistant Brown Norway BN/SsNHsdMcwi (BN) rat into the genomic background of the Dahl salt-sensitive SS/JrHsdMcwi (SS) rat attenuates the development of salt-sensitive hypertension and renal damage. To identify the regions within Chromosome 13 that attenuate the development of hypertension during a high-salt diet in the SS rat, we phenotyped a series of overlapping congenic lines covering Chromosome 13, generated from an intercross between the consomic SS-13BN rat and the SS rat. Blood pressure was determined in chronically catheterized rats after 2 wk of high-salt diet (8% NaCl) together with microalbuminuria as an index of renal damage. Four discrete regions were identified, ranging in size from 4.5 to 16 Mbp, each of which independently provided significant protection from hypertension during high-salt diet, reducing blood pressure by 20–29 mmHg. Protection was more robust in female than male rats in some of the congenic str...
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multiple blood pressure loci on rat Chromosome 13 attenuate development of hypertension in the dahl s hypertensive rat
Physiological Genomics, 2007Co-Authors: Carol Moreno, Howard J Jacob, Jozef Lazar, Mary L Kaldunski, Tao Wang, Richard J Roman, Andrew S Greene, Allen W CowleyAbstract:Previous studies have indicated that substitution of Chromosome 13 of the salt-resistant Brown Norway BN/SsNHsdMcwi (BN) rat into the genomic background of the Dahl salt-sensitive SS/JrHsdMcwi (SS)...
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brown norway Chromosome 13 confers protection from high salt to consomic dahl s rat
Hypertension, 2001Co-Authors: Allen W Cowley, Mary L Kaldunski, Richard J Roman, Andrew S Greene, Pierre Dumas, Jeffrey G Dickhout, Howard J JacobAbstract:Consomic rats (SS.BN13), in which Chromosome 13 from normotensive inbred Brown Norway rats from a colony maintained at the Medical College of Wisconsin (BN/Mcw) was introgressed into the background of Dahl salt-sensitive (SS/Mcw) rats, also maintained in a colony at the Medical College of Wisconsin, were bred. The present studies determined the mean arterial pressure (MAP) responses to salt and renal and peripheral vascular responses to norepinephrine and angiotensin II; 24-hour protein excretion and histological analyses were used to assess renal pathology in rats that received a high salt (4% NaCl) diet for 4 weeks. MAP of rats measured daily during the fourth week averaged 170±3.3 mm Hg in SS/Mcw rats, 119±2.1 mm Hg in SS.BN13 rats, and 103±1.3 mm Hg in BN/Mcw rats. After salt depletion, MAP fell an average of 27±4.5 mm Hg in SS/Mcw rats, 9±2.6 mm Hg in SS.BN13 rats, and 11±3.0 mm Hg in BN/Mcw rats. Protein excretion of SS/Mcw rats on a high salt diet averaged 189±30 mg/24 h, 63±18 mg/24 h in SS.BN13 rats, and 40±6.4 mg/24 h in BN/Mcw rats. Compared with SS.BN13 and BN/Mcw rats, SS/Mcw rats exhibited significantly greater increases of renal vascular resistance in response to intravenous norepinephrine and angiotensin II. Severe medullary interstitial fibrosis and tubular necrosis after a high salt diet were found consistently in SS/Mcw rat kidneys but were largely absent in the SS.BN13 and BN/Mcw rat kidneys. A similar degree of glomerular sclerosis was found in both SS/Mcw and SS.BN13 rats. In rats fed a 0.4% salt diet, the glomerular filtration rate of SS/Mcw rats was significantly less than that of BN/Mcw and SS.BN13 rats. These results reveal a powerful gene, or set of genes, within Chromosome 13 of BN/Mcw rats that confers protection from the detrimental effects of high salt to the SS/Mcw rats.
Guido Tricot - One of the best experts on this subject based on the ideXlab platform.
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Chromosome 13 deletion hypodiploidy and prognosis in multiple myeloma patients
Leukemia & Lymphoma, 2004Co-Authors: Athanasios Fassas, Guido TricotAbstract:The application of high-dose treatment with autologous stem cell transplant(s) has improved survival, when compared to standard treatment, in patients with multiple myeloma. However, this benefit is mostly enjoyed by specific patient subgroups characterized by the absence of high-risk disease features. High-risk features are, first and foremost, the detection of unfavorable cytogenetic abnormalities (Chromosome 13 deletion, hypodiploidy and myelodysplastic-type abnormalities in an otherwise typical myeloma karyotype) prior to treatment; elevated serum lactate dehydrogenase and C-reactive protein levels at diagnosis and high beta-2 microglobulin levels prior to transplant also convey poor prognosis, although they account for less variability of the observed outcome than the cytogenetic abnormalities. While high-dose treatment with autologous stem cell transplant(s) can cure a sizable minority of patients with low-risk disease features and significantly prolongs survival in others with similar characteristics, patients with high-risk features are virtually incurable and their survival benefit is much less pronounced. As the tremendous clinical variability of myeloma can now be traced to its underlying genetic abnormalities, routine cytogenetic analysis at diagnosis and relapse are absolutely indicated. Based on this stratification, high-risk patients are excellent candidates for novel therapeutic approaches, such as planned non-myeloablative allogeneic transplants following an autologous transplant.
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both hypodiploidy and deletion of Chromosome 13 independently confer poor prognosis in multiple myeloma
British Journal of Haematology, 2002Co-Authors: Athanasios Fassas, Jeffrey R Sawyer, Christopher Morris, Bart Barlogie, Tray Spencer, Maurizio Zangari, Choonkee Lee, Elias Anaissie, Firas Muwalla, Guido TricotAbstract:Summary. Complete or partial deletion of Chromosome 13 or translocations involving 13q (Δ13) by conventional cytogenetic analysis confers a poor prognosis in multiple myeloma (MM) patients, even with timely application of tandem autologous transplants. It was recently suggested that the prognostic significance of Δ13 is related to its frequent association with hypodiploidy but by itself does not have a poor prognostic significance. We therefore analysed our experience in 1475 consecutive MM patients in whom we intended treatment with tandem transplants after a melphalan-based conditioning regimen. Patients with abnormal cytogenetic analysis were grouped into hypodiploid/hypotetraploid, pseudodiploid and hyperdiploid groups, according to their modal Chromosome number. Their event-free and overall survival were compared with those of patients with a normalkaryotype. Both hypodiploidy and Δ13 were found to independently confer poor prognosis in MM patients. Furthermore, these parameters in combination with easily obtained pretransplant levels of β-2 microglobulin and albumin define three groups of MM patients with clearly distinct outcomes.
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both hypodiploidy and deletion of Chromosome 13 independently confer poor prognosis in multiple myeloma
British Journal of Haematology, 2002Co-Authors: Athanasios Fassas, Jeffrey R Sawyer, Christopher Morris, Bart Barlogie, Tray Spencer, Maurizio Zangari, Choonkee Lee, Elias Anaissie, Firas Muwalla, Guido TricotAbstract:Complete or partial deletion of Chromosome 13 or translocations involving 13q (delta13) by conventional cytogenetic analysis confers a poor prognosis in multiple myeloma (MM) patients, even with timely application of tandem autologous transplants. It was recently suggested that the prognostic significance of delta13 is related to its frequent association with hypodiploidy but by itself does not have a poor prognostic significance. We therefore analysed our experience in 1475 consecutive MM patients in whom we intended treatment with tandem transplants after a melphalan-based conditioning regimen. Patients with abnormal cytogenetic analysis were grouped into hypodiploid/hypotetraploid, pseudodiploid and hyperdiploid groups, according to their modal Chromosome number. Their event-free and overall survival were compared with those of patients with a normalkaryotype. Both hypodiploidy and delta13 were found to independently confer poor prognosis in MM patients. Furthermore, these parameters in combination with easily obtained pretransplant levels of beta-2 microglobulin and albumin define three groups of MM patients with clearly distinct outcomes.
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high incidence of Chromosome 13 deletion in multiple myeloma detected by multiprobe interphase fish
Blood, 2000Co-Authors: John D Shaughnessy, Erming Tian, Jeffrey R Sawyer, Klaus Bumm, Reid D Landes, Ashraf Badros, Christopher Morris, Guido Tricot, Joshua Epstein, Bart BarlogieAbstract:Multiple myeloma (MM) is a hypoproliferative malignancy yielding informative karyotypes in no more than 30% of newly diagnosed cases. Although cytogenetic and molecular deletion of Chromosome 13 is associated with poor prognosis, a MM tumor suppressor gene (TSG) has not been identified. To localize a minimal deleted region of Chromosome 13, clonotypic plasma cells from 50 consecutive patients with MM were subjected to interphase fluorescence in situ hybridization (FISH) analysis using a panel of 11 probes spanning the entire long arm of Chromosome 13. Whereas Chromosome 13 abnormalities were absent in plasma cells from 25 normal donors, 86% of patients with MM demonstrated such aberrations. Heterogeneity, both in deletion frequency and extent, was confirmed by simultaneous FISH with 2 Chromosome 13 probes. Deletion hot spots were noted at D13S272 (70%) and D13S31 (64%), 2 unlinked loci at 13q14. Homozygous deletions at these loci occurred in 12% (simultaneously in 8%) of the cases. Molecular deletions were found in all 14 patients with morphologic deletions, in 21 of 24 with uninformative karyotypes, and 8 of 12 patients with karyotype abnormalities lacking Chromosome 13 deletion. Homozygous deletion of any marker was noted in 4% with low and in 36% with higher plasma cell labeling index greater than 0.4% ( P = .01). The absence of increasing deletion incidence and extent with therapy duration suggests that the observed lesions are not induced by treatment. The high incidence and extent of Chromosome 13 deletions require the correlation of specific deletion(s) with poor prognosis. These analyses will provide valuable guidance toward cloning of an MM-TSG.
Howard J Jacob - One of the best experts on this subject based on the ideXlab platform.
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narrowing a region on rat Chromosome 13 that protects against hypertension in dahl ss 13bn congenic strains
American Journal of Physiology-heart and Circulatory Physiology, 2011Co-Authors: Carol Moreno, Howard J Jacob, Jan M Williams, Mingyu Liang, Jozef Lazar, Limin Lu, Allen W CowleyAbstract:Transfer of Chromosome 13 from the Brown Norway (BN) rat onto the Dahl salt-sensitive (SS) genetic background attenuates the development of hypertension, but the genes involved remain to be identified. The purpose of the present study was to confirm by telemetry that a congenic strain [SS.BN-(D13Hmgc37-D13Got22)/Mcwi, line 5], carrying a 13.4-Mb segment of BN Chromosome 13 from position 32.4 to 45.8 Mb, is protected from the development of hypertension and then to narrow the region of interest by creating and phenotyping 11 additional subcongenic strains. Mean arterial pressure (MAP) rose from 118 ± 1 to 186 ± 5 mmHg in SS rats fed a high-salt diet (8.0% NaCl) for 3 wk. Protein excretion increased from 56 ± 11 to 365 ± 37 mg/day. In contrast, MAP only increased to 152 ± 9 mmHg in the line 5 congenic strain. Six subcongenic strains carrying segments of BN Chromosome 13 from 32.4 and 38.2 Mb and from 39.9 to 45.8 Mb were not protected from the development of hypertension. In contrast, MAP was reduced by ∼30 mmHg in five strains, carrying a 1.9-Mb common segment of BN Chromosome 13 from 38.5 to 40.4 Mb. Proteinuria was reduced by ∼50% in these strains. Sequencing studies did not identify any nonsynonymous single nucleotide polymorphisms in the coding region of the genes in this region. RT-PCR studies indicated that 4 of the 13 genes in this region were differentially expressed in the kidney of two subcongenic strains that were partially protected from hypertension vs. those that were not. These results narrow the region of interest on Chromosome 13 from 13.4 Mb (159 genes) to a 1.9-Mb segment containing only 13 genes, of which 4 are differentially expressed in strains partially protected from the development of hypertension.
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multiple blood pressure loci on rat Chromosome 13 attenuate development of hypertension in the dahl s hypertensive rat
Physiological Genomics, 2007Co-Authors: Carol Moreno, Howard J Jacob, Jozef Lazar, Mary L Kaldunski, Tao Wang, Richard J Roman, Andrew S Greene, Allen W CowleyAbstract:Previous studies have indicated that substitution of Chromosome 13 of the salt-resistant Brown Norway BN/SsNHsdMcwi (BN) rat into the genomic background of the Dahl salt-sensitive SS/JrHsdMcwi (SS) rat attenuates the development of salt-sensitive hypertension and renal damage. To identify the regions within Chromosome 13 that attenuate the development of hypertension during a high-salt diet in the SS rat, we phenotyped a series of overlapping congenic lines covering Chromosome 13, generated from an intercross between the consomic SS-13BN rat and the SS rat. Blood pressure was determined in chronically catheterized rats after 2 wk of high-salt diet (8% NaCl) together with microalbuminuria as an index of renal damage. Four discrete regions were identified, ranging in size from 4.5 to 16 Mbp, each of which independently provided significant protection from hypertension during high-salt diet, reducing blood pressure by 20–29 mmHg. Protection was more robust in female than male rats in some of the congenic str...
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multiple blood pressure loci on rat Chromosome 13 attenuate development of hypertension in the dahl s hypertensive rat
Physiological Genomics, 2007Co-Authors: Carol Moreno, Howard J Jacob, Jozef Lazar, Mary L Kaldunski, Tao Wang, Richard J Roman, Andrew S Greene, Allen W CowleyAbstract:Previous studies have indicated that substitution of Chromosome 13 of the salt-resistant Brown Norway BN/SsNHsdMcwi (BN) rat into the genomic background of the Dahl salt-sensitive SS/JrHsdMcwi (SS)...
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brown norway Chromosome 13 confers protection from high salt to consomic dahl s rat
Hypertension, 2001Co-Authors: Allen W Cowley, Mary L Kaldunski, Richard J Roman, Andrew S Greene, Pierre Dumas, Jeffrey G Dickhout, Howard J JacobAbstract:Consomic rats (SS.BN13), in which Chromosome 13 from normotensive inbred Brown Norway rats from a colony maintained at the Medical College of Wisconsin (BN/Mcw) was introgressed into the background of Dahl salt-sensitive (SS/Mcw) rats, also maintained in a colony at the Medical College of Wisconsin, were bred. The present studies determined the mean arterial pressure (MAP) responses to salt and renal and peripheral vascular responses to norepinephrine and angiotensin II; 24-hour protein excretion and histological analyses were used to assess renal pathology in rats that received a high salt (4% NaCl) diet for 4 weeks. MAP of rats measured daily during the fourth week averaged 170±3.3 mm Hg in SS/Mcw rats, 119±2.1 mm Hg in SS.BN13 rats, and 103±1.3 mm Hg in BN/Mcw rats. After salt depletion, MAP fell an average of 27±4.5 mm Hg in SS/Mcw rats, 9±2.6 mm Hg in SS.BN13 rats, and 11±3.0 mm Hg in BN/Mcw rats. Protein excretion of SS/Mcw rats on a high salt diet averaged 189±30 mg/24 h, 63±18 mg/24 h in SS.BN13 rats, and 40±6.4 mg/24 h in BN/Mcw rats. Compared with SS.BN13 and BN/Mcw rats, SS/Mcw rats exhibited significantly greater increases of renal vascular resistance in response to intravenous norepinephrine and angiotensin II. Severe medullary interstitial fibrosis and tubular necrosis after a high salt diet were found consistently in SS/Mcw rat kidneys but were largely absent in the SS.BN13 and BN/Mcw rat kidneys. A similar degree of glomerular sclerosis was found in both SS/Mcw and SS.BN13 rats. In rats fed a 0.4% salt diet, the glomerular filtration rate of SS/Mcw rats was significantly less than that of BN/Mcw and SS.BN13 rats. These results reveal a powerful gene, or set of genes, within Chromosome 13 of BN/Mcw rats that confers protection from the detrimental effects of high salt to the SS/Mcw rats.
Abraham Aviv - One of the best experts on this subject based on the ideXlab platform.
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survival advantage of cultured human vascular endothelial cells that lost Chromosome 13
Chromosoma, 2004Co-Authors: Masayuki Kimura, Smita S Patel, Abraham AvivAbstract:We explored the nature of Chromosome 13 loss in cultured human vascular endothelial cells (HUVECs). Chromosome 13 loss detected by metaphase and interphase analysis was noted in earlier passages of HUVEC strains with no relation to telomere length or replicative senescence. Ectopic expression of telomerase did not influence the loss of Chromosome 13. HUVECs losing Chromosome 13 demonstrated increased migratory potential and loss of heterozygosity. Collectively, these observations suggest that the loss of Chromosome 13 gives cultured HUVECs a replicative advantage.
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loss of Chromosome 13 in cultured human vascular endothelial cells
Experimental Cell Research, 2000Co-Authors: Li Zhang, Masayuki Kimura, Smita S Patel, Hana Aviv, Jeffrey P Gardner, Koji Okuda, Arlene Bardeguez, Abraham AvivAbstract:Abstract In the vascular endothelium of human beings, telomere length is negatively related while the frequency of aneuploidy is positively related to donor age. Both in culture and in vivo the frequency of aneuploidy increases as telomere length is shortened. In this study we explored the relation between telomere length and aneuploidy in cultured human umbilical vein endothelial cells (HUVEC) by: (a) karyotype analysis and fluorescent in situ hybridization (FISH), (b) measurement of the terminal restriction fragments (TRF), and (c) assessment of replicative senescence by the expression of β-galactosidase. Of 8 HUVEC strains, 7 cell strains lost Chromosome 13, as shown by metaphase analysis and FISH of interphase cells. Five strains gained Chromosome 11. In addition, five HUVEC strains became hypotetraploid shortly after the loss of Chromosome 13. The loss of Chromosome 13 was observed as early as PD 20, when mean TRF length was greater than 9 kb and the percentage of cells positive for β-galactosidase was relatively low. The almost uniform loss of Chromosome 13 suggests that this unique type of aneuploidy of HUVEC is the result of a progressive expression of clones with survival advantage.
Carol Moreno - One of the best experts on this subject based on the ideXlab platform.
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narrowing a region on rat Chromosome 13 that protects against hypertension in dahl ss 13bn congenic strains
American Journal of Physiology-heart and Circulatory Physiology, 2011Co-Authors: Carol Moreno, Howard J Jacob, Jan M Williams, Mingyu Liang, Jozef Lazar, Limin Lu, Allen W CowleyAbstract:Transfer of Chromosome 13 from the Brown Norway (BN) rat onto the Dahl salt-sensitive (SS) genetic background attenuates the development of hypertension, but the genes involved remain to be identified. The purpose of the present study was to confirm by telemetry that a congenic strain [SS.BN-(D13Hmgc37-D13Got22)/Mcwi, line 5], carrying a 13.4-Mb segment of BN Chromosome 13 from position 32.4 to 45.8 Mb, is protected from the development of hypertension and then to narrow the region of interest by creating and phenotyping 11 additional subcongenic strains. Mean arterial pressure (MAP) rose from 118 ± 1 to 186 ± 5 mmHg in SS rats fed a high-salt diet (8.0% NaCl) for 3 wk. Protein excretion increased from 56 ± 11 to 365 ± 37 mg/day. In contrast, MAP only increased to 152 ± 9 mmHg in the line 5 congenic strain. Six subcongenic strains carrying segments of BN Chromosome 13 from 32.4 and 38.2 Mb and from 39.9 to 45.8 Mb were not protected from the development of hypertension. In contrast, MAP was reduced by ∼30 mmHg in five strains, carrying a 1.9-Mb common segment of BN Chromosome 13 from 38.5 to 40.4 Mb. Proteinuria was reduced by ∼50% in these strains. Sequencing studies did not identify any nonsynonymous single nucleotide polymorphisms in the coding region of the genes in this region. RT-PCR studies indicated that 4 of the 13 genes in this region were differentially expressed in the kidney of two subcongenic strains that were partially protected from hypertension vs. those that were not. These results narrow the region of interest on Chromosome 13 from 13.4 Mb (159 genes) to a 1.9-Mb segment containing only 13 genes, of which 4 are differentially expressed in strains partially protected from the development of hypertension.
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mechanism of differential cardiovascular response to propofol in dahl salt sensitive brown norway and Chromosome 13 substituted consomic rat strains role of large conductance ca2 and voltage activated potassium channels
Journal of Pharmacology and Experimental Therapeutics, 2009Co-Authors: Anna Stadnicka, Carol Moreno, Richard J Roman, S J Contney, Dorothee Weihrauch, Zeljko J Bosnjak, Thomas A StekielAbstract:Cardiovascular sensitivity to general anesthetics is highly variable among individuals in both human and animal models, but little is known about the genetic determinants of drug response to anesthetics. Recently, we reported that propofol (2,6-diisopropylphenol) causes circulatory instability in Dahl salt-sensitive SS/JRHsdMcwi (SS) rats but not in Brown Norway BN/NHsdMcwi (BN) rats and that these effects are related to genes on Chromosome 13. Based on the hypothesis that propofol does target mesenteric circulation, we investigated propofol modulation of mesenteric arterial smooth muscle cells (MASMC) in SS and BN rats. The role of Chromosome 13 was tested using SS-13BN/Mcwi and BN-13SS/Mcwi consomic strains with Chromosome 13 substitution. Propofol (5 μM) produced a greater in situ hyperpolarization of MASMC membrane potential in SS than BN rats, and this effect was abrogated by iberiotoxin, a voltage-activated potassium (BK) channel blocker. In inside-out patches, the BK channel number, Po, and apparent Ca2+ sensitivity, and propofol sensitivity all were significantly greater in MASMC of SS rats. The density of whole-cell BK current was increased by propofol more in SS than BN myocytes. Immunolabeling confirmed higher expression of BK α subunit in MASMC of SS rats. Furthermore, the hyperpolarization produced by propofol, the BK channel properties, and propofol sensitivity were modified in MASMC of SS-13BN/Mcwi and BN-13SS/Mcwi strains toward the values observed in the background SS and BN strains. We conclude that differential function and expression of BK channels, resulting from genetic variation within Chromosome 13, contribute to the enhanced propofol sensitivity in SS and BN-13SS/Mcwi versus BN and SS-13BN/Mcwi strains.
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multiple blood pressure loci on rat Chromosome 13 attenuate development of hypertension in the dahl s hypertensive rat
Physiological Genomics, 2007Co-Authors: Carol Moreno, Howard J Jacob, Jozef Lazar, Mary L Kaldunski, Tao Wang, Richard J Roman, Andrew S Greene, Allen W CowleyAbstract:Previous studies have indicated that substitution of Chromosome 13 of the salt-resistant Brown Norway BN/SsNHsdMcwi (BN) rat into the genomic background of the Dahl salt-sensitive SS/JrHsdMcwi (SS) rat attenuates the development of salt-sensitive hypertension and renal damage. To identify the regions within Chromosome 13 that attenuate the development of hypertension during a high-salt diet in the SS rat, we phenotyped a series of overlapping congenic lines covering Chromosome 13, generated from an intercross between the consomic SS-13BN rat and the SS rat. Blood pressure was determined in chronically catheterized rats after 2 wk of high-salt diet (8% NaCl) together with microalbuminuria as an index of renal damage. Four discrete regions were identified, ranging in size from 4.5 to 16 Mbp, each of which independently provided significant protection from hypertension during high-salt diet, reducing blood pressure by 20–29 mmHg. Protection was more robust in female than male rats in some of the congenic str...
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multiple blood pressure loci on rat Chromosome 13 attenuate development of hypertension in the dahl s hypertensive rat
Physiological Genomics, 2007Co-Authors: Carol Moreno, Howard J Jacob, Jozef Lazar, Mary L Kaldunski, Tao Wang, Richard J Roman, Andrew S Greene, Allen W CowleyAbstract:Previous studies have indicated that substitution of Chromosome 13 of the salt-resistant Brown Norway BN/SsNHsdMcwi (BN) rat into the genomic background of the Dahl salt-sensitive SS/JrHsdMcwi (SS)...