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1
Garrett, Michael R. "Genetic dissection of hypertension-related renal disease using the Dahl salt-sensitive rat." Connect to Online Resource-OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1175545256.
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Dissertation (Ph.D.)--University of Toledo, 2006."In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 89-95, p. 127-131, p. 184-192, p.198-233.
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Garrett, Michael Richard. "Genetic Dissection of Hypertension Related Renal Disease Using the Dahl Salt-Sensitive Rat." University of Toledo Health Science Campus / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=mco1175545256.
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NAGATA, KOHZO, TOYOAKI MUROHARA, XIAN WU CHENG, SHOGO WATANABE, MASAAKI MIYACHI, MAYUKO OHTAKE, MIWA TAKATSU, et al. "Glucocorticoids Activate Cardiac Mineralocorticoid Receptors in Adrenalectomized Dahl Salt- Sensitive Rats." Nagoya University School of Medicine, 2014. http://hdl.handle.net/2237/19484.
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Zhao, Xigeng. "The renin-angiotensin system, cardiac hypertrophy, and salt-sensitive hypertension in Dahl rats." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0018/MQ57170.pdf.
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Gabor, Alexander. "Role of Angiotensin II, Glutamate, Nitric Oxide and an Aldosterone-ouabain Pathway in the PVN in Salt-induced Pressor Responses in Rats." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/22900.
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High salt intake contributes to the development of hypertension in salt-sensitive humans and animals and the mechanistic causes are poorly understood. In Dahl salt-sensitive (S) but not salt-resistant (R) rats, high salt diet increases cerebrospinal fluid (CSF) [Na+] and activates an aldosterone-mineralocorticoid receptor-epithelial sodium channel-endogenous ouabain (MR-ENaC-EO) neuromodulatory pathway in the brain that enhances the activity of sympatho-excitatory angiotensinergic and glutamatergic pathways, leading to an increase in sympathetic nerve activity (SNA) and blood pressure (BP). We hypothesize that high salt diet in Dahl S rats enhances Ang II release in the paraventricular nucleus (PVN), causing a decrease in local nitric oxide (NO) action and an increase in local glutamate release thereby elevating SNA, BP and heart rate (HR). The present study evaluated the effects of agonists or blockers of MR, ENaC, EO, nitric oxide synthase (NOS) or glutamate and AT1-receptors on the BP and HR responses to acute infusions of Na+ rich aCSF, intracerebroventricularly (icv), or in the PVN of Dahl S, R or Wistar rats or to high salt diet in Dahl S and R rats. In Wistar rats, aldosterone in the PVN enhanced the BP and HR responses to infusion of Na+ rich aCSF in the PVN, but not in the CSF, and only the enhancement was prevented by blockers of MR, ENaC and EO in the PVN. AT1-receptor blockers in the PVN fully blocked the enhancement by aldosterone and the responses to infusion of Na+ rich aCSF icv, or in the PVN. Na+ rich aCSF in the PVN caused larger increases in BP and HR in Dahl S vs. R rats and the responses to Na+ were fully blocked by an AT1-receptor blocker in the PVN. BP and HR responses to a NOS blocker in the PVN were the same, but L-NAME enhanced Na+ effects more in Dahl R than S rats. High salt diet attenuated increases in BP from L-NAME in the PVN of Dahl S but not R rats. AT1 and glutamate receptor blockers candesartan and kynurenate in the PVN decreased BP in Dahl S but not R rats on high salt diet. At the peak BP response to candesartan, kynurenate in the PVN further decreased BP whereas candesartan did not further decrease BP at the peak BP response to kynurenate. Our findings indicate that both an acute increase in CSF [Na+] and high salt intake in Dahl S rats increases AT1-receptor activation and decreases NO action in the PVN thereby contributing to the pressor responses to Na+ and presumably, to dietary salt-induced hypertension. The increased BP response to AT1-receptor activation in the PVN of Dahl S is mediated by enhanced local glutamate receptor activation. An MR-ENaC-EO pathway in the PVN can be functionally active and further studies need to assess its role in Dahl S rats on high salt intake.
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Jones, Rowdy, Jacqueline C. Potter, Shannon C. Allenn, Conor B. Miles, Rhesa Dykes, Michelle M. Duffourc, and Aaron J. Polichnowski. "Striking differences in uromodulin excretion and expression, salt-sensitive hypertension, and renal injury in Dahl SS vs. BN and SS.BN1 consomic rats." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/123.
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Uromodulin (UMOD) is a protein made exclusively in the thick ascending limb. Clinical studies have demonstrated that rare missense mutations in UMOD result in autosomal dominant tubulointerstitial kidney diseases manifest by tubulointerstitial fibrosis (TIF), tubular cysts and a rapid progression to renal failure. In addition, several genome wide association studies reported that common single nucleotide polymorphisms in the UMOD gene are associated with an increased risk of chronic kidney disease (CKD) and hypertension. Interestingly, Dahl salt-sensitive (SS) rats exhibit many of the same pathologies observed in these clinical populations with alterations in UMOD.
The goal of this study was to assess the qualitative and quantitative aspects of UMOD via western blotting, and the extent of SS hypertension and proteinuria in Dahl SS vs. a consomic rat strain in which chromosome 1 of the salt-resistant Brown-Norway (BN) rat, harboring the UMOD gene, has been introgressed into the Dahl SS background (SS.BN1). We hypothesized that differences in UMOD would be apparent in SS vs. SS.BN1 rats maintained on a low salt-diet and that the extent of SS hypertension and proteinuria would be attenuated in SS.BN1 vs SS rats. Western blot of urinary UMOD was performed in 16 week old SS (n=5), SS.BN1 (n=7) and BN (n=6) rats maintained on a low salt (LS) diet. BP (radiotelemetry) and proteinuria were assessed during LS feeding and during three weeks of high salt (HS) feeding in a different group of 8-10 week old SS (n=9) and SS.BN1 (n=8) rats.
For western blotting, urine was normalized based on the protein concentration, and the density of the 85 kDa UMOD band in SS and SS.BN1 samples were normalized to the average density observed in BN rats. The UMOD band was 4.5 fold higher (p
In summary, these data demonstrate striking qualitative and quantitative differences in UMOD between SS and SS.BN1 rats. The pattern of UMOD expression in SS rats is consistent with that observed in some patient populations of UMOD associated kidney disease. Finally, the evidence that SS.BN1 rats, harboring the UMOD gene from BN rats, exhibit significant protection against SS hypertension and proteinuria is consistent with the notion that an alteration in UMOD function may, in part, be responsible for such pathologies in SS rats.
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Breidenbach, Joshua David. "The Development of a Novel Model for Chronic Renal Allograft Rejection." University of Toledo Health Science Campus / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=mco1533298235487342.
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Gadkari, Tushar V. "Effect of Arginine and Oscillatory Ca2+ on Vascular Response Mediated Via Nitric Oxide Signaling in Normal and Salt Sensitive Hypertensive Rat Mesenteric Arterioles." FIU Digital Commons, 2013. http://digitalcommons.fiu.edu/etd/891.
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Hypertension, a major risk factor in the cardiovascular system, is characterized by an increase in the arterial blood pressure. High dietary sodium is linked to multiple cardiovascular disorders including hypertension. Salt sensitivity, a measure of how the blood pressure responds to salt intake is observed in more than 50% of the hypertension cases. Nitric Oxide (NO), as an endogenous vasodilator serves many important biological roles in the cardiovascular physiology including blood pressure regulation. The physiological concentrations for NO bioactivity are reported to be in 0-500 nM range. Notably, the vascular response to NO is highly regulated within a small concentration spectrum. Hence, much uncertainty surrounds how NO modulates diverse signaling mechanisms to initiate vascular relaxation and alleviate hypertension.
Regulating the availability of NO in the vasculature has demonstrated vasoprotective effects. In addition, modulating the NO release by different means has proved to restore endothelial function. In this study we addressed parameters that regulated NO release in the vasculature, in physiology and pathophysiology such as salt sensitive hypertension. We showed that, in the rat mesenteric arterioles, Ca2+ induced rapid relaxation (time constants 20.8 ± 2.2 sec) followed with a much slower constriction after subsequent removal of the stimulus (time constants 104.8 ± 10.0 sec). An interesting observation was that a fourfold increase in the Ca2+ frequency improved the efficacy of arteriolar relaxation by 61.1%. Our results suggested that, Ca2+ frequency-dependent transient release of NO from the endothelium carried encoded information; which could be translated into different steady state vascular tone. Further, Agmatine, a metabolite of L-arginine, as a ligand, was observed to relax the mesenteric arterioles. These relaxations were NO-dependent and occurred via α-2 receptor activity. The observed potency of agmatine (EC50, 138.7 ± 12.1 µM; n=22), was 40 fold higher than L-arginine itself (EC50, 18.3 ± 1.3 mM; n = 5). This suggested us to propose alternative parallel mechanism for L-arginine mediated vascular relaxation via arginine decarboxylase activity. In addition, the biomechanics of rat mesentery is important in regulation of vascular tone. We developed 2D finite element models that described the vascular mechanics of rat mesentery. With an inverse estimation approach, we identified the elasticity parameters characterizing alterations in normotensive and hypertensive Dahl rats.
Our efforts were towards guiding current studies that optimized cardiovascular intervention and assisted in the development of new therapeutic strategies. These observations may have significant implications towards alternatives to present methods for NO delivery as a therapeutic target. Our work shall prove to be beneficial in assisting the delivery of NO in the vasculature thus minimizing the cardiovascular risk in handling abnormalities, such as hypertension.
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Dutil, Julie. "Identification of blood pressure genes in the Dahl salt-sensitive hypertension model." Thèse, 2005. http://hdl.handle.net/1866/15570.
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Hao, Jing-Ming. "Differences in the expression of opioid peptides in Dahl salt-resistant and salt-sensitive rats." Thesis, 1993. http://hdl.handle.net/2429/1763.
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The Dahl strain of genetically salt-resistant (R) and salt-sensitive (S) rats affords an opportunity to explore mechanisms for the development of hypertension and the consequences, as well as sensitivity or resistance, of salt-induced hypertension. Because of the evidence that opioid peptides and their receptors can be involved in cardiovascular regulation, the objective of this study was to test the hypothesis that /3-endorphin and enkephalins are involved in the development of hypertension through the determination of their precursors preproopiomelanocortin (POMC) and preproenkephalin (ppENK) messenger RNAs in this animal model. Three week old inbred Dahl R and S rats were maintained on high salt diet (8% NaCI) or low salt diet (0.4%) for six weeks. POMCmRNA and ppenk mRNA were examined from tissues of Dahl R and S rats as determinedly Northern blot analysis using p-actin as an internal standard. POMC mRNA was abundant in the pituitary tissues and was not detectable in other tissues. ppenk mRNA was abundantly present in brain, testis and heart. There was more POMC mRNA in the pituitary tissue of R rats on high salt diet compared with the pituitary of S rats on high salt diet. Differences in POMC mRNA in the pituitary were not observed between R and S on low salt diet. There were no differences of ppENK mRNA in the brain between R and S rats on high salt diet. Increased ppENK mRNA was found in the right and left ventricles of the heart of S rats on low salt diet. The increase in ppENK mRNA in the cardiac ventricles of S rats was exaggerated when they were on high salt diet. To define the role of increased ppENK mRNA in the S rats in the regulation of cardiovascular function, the effects of intravenous administration of proenkephalin-derived bioactive peptides Leu5-enkephalin (LE), Met5-enkephalin (ME), Met5-enkephalin-Arg6-Gly7-Leu5 (MEAGL), andMet5-enkephalin-Ard-Phe7 (MEAP) in Sprague-Dawley rats, and effects of these peptides on isolated intact hearts of Sprague-Dawley rats, were examined. At intravenous doses of 3.6 and 36 nmole, none of the opioid peptides had effects on arterial pressure or heart rate. Intravenous administration of LE, ME, MEAGL or MEAP at a dose of 360 nmole per animal briefly deceased the heart rate. The MEAP, but not LE, ME, or MEAGL, induced a more prolonged increase in arterial pressure at the intravenous dose of 360 nmole. LE,ME, MEAGL or MEAP, at concentration 10-6 M in the perfusion solution, had no direct effect on the developed pressure in the left ventricle of the isolated heart. These data show increased preproenkephalin mRNA in the heart and decreased POMC mRNA in the pituitary of Dahl S compared to Dahl R rats. From these results we speculate that: (1)inefficient pituitary production of POMC and consequently J3-endorphin, which is known to decrease arterial pressure, may contribute to the development of hypertension in the S rats on high salt diet; (2) increased release from the heart of the opioid peptide MEAP, and possibly other enkephalins, may be related to the high blood pressure of S rats on low salt diet; (3) exaggerated release of MEAP and/or other enkephalins may exacerbate the process of hypertension in S rats on high salt diet.
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Palijan, Ana. "Étude d'un locus pour trait quantitatif de l'hypertension sur le chromosome 3 du rat Dahl Salt-Sensitive." Thèse, 2004. http://hdl.handle.net/1866/15528.
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Payne, Geoffrey Wallace. "The characterization of cerebrovascular dysfunction associated with hypertensive encephalopathy in Dahl salt-sensitive rats /." 2003.
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Duong, Chenda. "Localisation de loci à trait quantitatif pour l'hypertension sur les chromosomes 17 et 16 du rat Dahl Salt-Sensitive." Thèse, 2007. http://hdl.handle.net/1866/7621.
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Moujahidine, Myriam. "Localisation d'un locus pour trait quantitatif pour l'hypertension sur les chromosomes 16 et 17 du rat Dahl Salt-Sensitive." Thèse, 2003. http://hdl.handle.net/1866/14652.
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Eliopoulos, Vasiliki. "Localisation d'un locus pour trait quantitif pour l'hypertension sur le chromosome 2 du rat Dahl." Thèse, 2006. http://hdl.handle.net/1866/15582.
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Lambert, Raphaëlle. "Localisation d'un locus pour trait quantitatif pour l'hypertension sur le chromosome 18 du rat Dahl." Thèse, 2005. http://hdl.handle.net/1866/15554.
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Hariram, Arvind. "An immunohistochemical evaluation of the effect of salt (NaCI) on adrenal adrenomedullin content in Dahl rats." Thesis, 2003. http://hdl.handle.net/10413/2760.
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Adrenomedullin (ADM) is a 52 amino acid vasodilator peptide isolated, in 1993, from human pheochromocytoma. It has been demonstrated in the adrenal medulla of several mammalian species, including humans and rats. There have been conflicting results of the tissue distribution in the adrenal cortex. Hypertension is a complex trait with multiple genetic and environmental influences. Furthermore, salt-sensitive hypertension is characterized by a cluster of renal, hormonal, and metabolic derangements that might favour the development of cardiovascular and renal complications. Therefore the objective of this study was to investigate the adrenal distribution of ADM as well as to semi-quantitatively assess the adrenomedullin secretory capacity of the adrenal gland in the rat model of salt sensitive hypertension. Fourty-four male weanling rats were divided into 4 experimental groups and placed on a dietary regimen for 6 weeks viz. Dahl salt sensitive (DSS) rats on a high sodium diet (8% NaCl), DSS on a normal sodium diet (1% NaCl) matched with normotensive Dahl salt resistant (DSR) rats on the same dietary treatments. Blood pressure was monitored by tail-cuff readings and by the end of the six weeks, the DSS rats developed hypertension with tachycardia irrespective of the diet they were fed. The normal sodium diet was found to delay the development of hypertension, whilst the high sodium diet exacerbated the development of hypertension. Kidney weights and heart weights were greater in DSS rats than DSR rats probably due to their renal pathology or cardiac hypertrophy. Adrenomedullin immunopositivity was found predominantly in the adrenal medulla, and to varying degrees in the zona glomerulosa and zona reticularis of the adrenal cortex. The semi-quantitative analysis indicate that there was a 6.3 fold increase in ADM content of DSS rats compared to the DSR rats, where both consumed the 1% NaCI supplemented diet (DSR : 5.98 ± 0.3 vs. DSS : 37.85 ± 0.5, PThesis (M.Sc.)-University of Durban-Westville, 2003.
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Sivo, Zsuzsa. "Analyse d'un locus pour trait quantitatif pour l'hypertension sur le chromosome 10 du rat Dahl." Thèse, 2002. http://hdl.handle.net/1866/14644.
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Charron, Sophie. "Localisation et caractère monogénique de cinq loci de traits quantitatifs de l'hypertension artérielle sur le chromosome 10 du rat Dahl salt-sensitive." Thèse, 2007. http://hdl.handle.net/1866/7624.
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Chauvet, Cristina. "Identification et regroupement de QTL influençant la pression artérielle en modules épistatiques et analyse de deux gènes candidats chez la souche Dahl Salt-Sensitive." Thèse, 2015. http://hdl.handle.net/1866/13525.
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Moreira, Jesse Daniel. "Neural mechanisms promoting G-alpha-i2 protein dependent salt sensitive hypertension in the Sprague-Dawley rat." Thesis, 2021. https://hdl.handle.net/2144/42560.
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Hypertension (HTN) is a critical public health issue estimated to contribute to 10% of deaths worldwide. Additionally, the salt sensitivity of blood pressure, an exaggerated pressor response to elevated dietary sodium intake, is estimated to be present in approximately 50% of the hypertensive population and 25% of the normotensive population. This is a critical problem as the average American consumes roughly three times the daily sodium intake recommended by the American Heart Association.
Our laboratory has previously identified a critical role of Hypothalamic Paraventricular Nucleus (PVN) Gαi2 proteins in the maintenance of salt resistance and normotension in the rat. Salt resistant rats such as the Sprague-Dawley (SD) rat site- specifically upregulate these proteins in response to elevated dietary sodium intake to facilitate sympathoinhibition, natriuresis, and normotension. In contrast, in the Dahl Salt Sensitive (DSS) rat, and in salt resistant rats in which this protein is experimentally downregulated, our laboratory has identified the development of renal nerve-dependent sympathoexcitation and salt-sensitive hypertension (ssHTN). However, the neural mechanisms whereby PVN Gαi2 proteins facilitate salt resistance are unclear. In addition, there is a robust literature in other rat models of HTN suggesting that both neuroinflammation in the PVN as well as an imbalance between PVN inhibitory GABAergic and excitatory glutamatergic signaling contribute to elevations in sympathetic outflow to promote HTN.
In this study, SD rats infused chronically with either targeted Gαi2 oligodeoxynucleotides (ODNs) or control scrambled (SCR) ODNs and challenged with either normal (0.6% NaCl) or high-salt (4% NaCl) diets were used to demonstrate that 1) PVN microglial activation and associated pro-inflammatory cytokine production contribute to the development of Gαi2 protein dependent ssHTN, 2) sex-dependent PVN microglial-mediated neuroinflammation precedes and likely drives the development of sympathoexcitation following high dietary sodium administration in male but not female Gαi2 protein dependent ssHTN, and 3) PVN GABAergic and glutamatergic signaling is disrupted and imbalanced, favoring excitation over inhibition, following elevated dietary sodium intake in Gαi2 protein dependent ssHTN. Together, these findings shed light on the pathological neural processes that occur in the absence of PVN Gαi2 protein upregulation and reveal potential mechanistic targets in the management of ssHTN.
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Fillion-Forté, Valérie. "Le syndrome métabolique chez les congéniques du rat Dahl : influence de la diète et rôle du récepteur de l'ANP." Thèse, 2010. http://hdl.handle.net/1866/4285.
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L’hypertension artérielle et l’obésité sont deux composantes conjointement reliées du syndrome métabolique. Les récepteurs de l’ANP (GCA) et de l’oxyde nitrique (GCs) ont des propriétés diurétiques, natriurétiques, vasodilatatrices et sont liés au contrôle de la pression. Des études récentes ont démontré leur implication dans l’obésité. Hypothèse : Une différence génétique au niveau du gène GCA pourrait contribuer à des différences physiologiques. La composante lipidique et/ou sodique de la diète pourrait influencer la fonction rénale, cardiaque et les valeurs anthropométriques différemment chez les souches congéniques. Objectifs : (1) Déterminer l’effet de la composante lipidique et sodique des diètes; (2) Évaluer l’influence de GCA sur la réponse physiologique des souches congéniques; (3) Expliquer les mécanismes physiologiques procurant une réduction de la pression artérielle chez la souche SM9. Méthodologie : Des modèles congéniques du rat Dahl (DSS) hypertendu, nourri avec une diète riche en gras (HF) ou normale (NF), ont été utilisés pour démontrer l’impact d’un segment chromosomique d’origine normotendue. Résultats : La souche SM9 a une prise de poids plus importante que SM12 et DSS sur diète HF malgré un apport alimentaire équivalent. La souche SM9 présente également un ratio masse adipeuse/masse maigre plus élevé que SM12 et DSS. Nous n’avons observé aucune augmentation de la pression artérielle en réponse à la diète HF pour les 3 souches malgré une augmentation du dommage rénal pour les 3 souches. Le dommage rénal est plus important chez DSS que pour les 2 congéniques. La réponse diurétique à l’ANP est plus élevée chez SM9 et est influencée par le contenu en sel dand la diète. La perte glomérulaire plus importante chez le rat DSS semble compensée par une augmentation de la réponse à l’ANP par les glomérules résiduels. Il y a une corrélation entre l’activité de GCA en réponse à l’ANP, les niveaux d’ARNm et le nombre de répétition du dinucléotide TA dans son promoteur. Le rat DSS présente une hypertrophie cardiaque plus importante que les deux souches congénique et ceci n’est pas modifié par la diète HF. Conclusion : Nos études ont permis de mettre en évidence un effet génétique impliquant le segment chromosomique normotendu contenant GCA dans la réponse à une diète HF chez le rat DSS.Hypertension and obesity are two related components of the metabolic syndrome. The ANP receptor (GCA) and nitric oxide receptor (sGC) have diuretic, natriuretic, vasodilatory properties, and are linked to blood pressure control. Furthermore a recent study has demonstrated the implication of GCA and sGC in the development of obesity. Hypothesis: A genetic difference in GCA gene could contribute to physiological differences. The differencial lipid and/or sodium composition of the diet could influence the renal, cardiac and anthropometric values. Objectives: (1) To determine the effect of fat and sodium on the physiological parameters; (2) To evaluate the influence of GCA on the physiological response of the congenic rat; (3) To explain the mechanisms of the blood pressure reduction in SM9 rats. Methodology: Congenic model of DSS rat, fed with either high fat (HF) or normal (NF) diet, were used to demonstrate the impact of a chromosome segment from normotensive origin on physiological functions. C2SM9 contains GCA and sGC from normotensive origin while C2SM12 harbours only sGC from normotensive origin. Results: HF diet had negative feature on body composition, renal damage, creatinine clearance and inhibited the diuretic/natriuretic effect of ANP. The normotensive segment including GCA and sGC has reduced the blood pressure, improve the renal damage and increased the diuretic/natriuretic capacity of SM9 in response to ANP injection when compared to SM12 and DSS. GCA mRNA and the clearance receptor ratio were reduced in SM9 in the renal cortex and retroperitoneal fat. SM12 and SM9, containing the chromosomal segment that includes sGC, improve their lipid profile compared with DSS. Conclusion: Our results suggested a compensatory increase in the GCA levels for SM12 and DSS that is insufficient to improve their pathophysiologic status as observed in SM9. HF diet increases the metabolic syndrome in those rats.