Project description:Elevated levels of an endogenous Na/K‐ATPase inhibitor marinobufagenin accompany salt‐sensitive hypertension and are implicated in cardiac fibrosis. Immunoneutralization of marinobufagenin reduces blood pressure in Dahl salt‐sensitive (Dahl‐S) rats. The effect of the anti‐marinobufagenin monoclonal antibody on blood pressure, left ventricular (LV) and renal remodeling, and LV gene expression were investigated in hypertensive Dahl‐S rats.
Project description:Salt-sensitive hypertension is a common form of hypertension characterized by an exaggerated blood pressure response to dietary salt intake. The molecular mechanisms linking salt-induced hypertension to multi-organ damage remain poorly defined. To address this issue, we generated a longitudinal multi-organ transcriptomic atlas by performing RNA sequencing on the kidney cortex, kidney medulla, liver, and heart across four stages of hypertension in male Dahl salt-sensitive rats. These data provide a valuable resource for identifying organ-specific transcriptional responses involved in the pathogenesis of salt-induced hypertension.
Project description:We analyzed the glomerular proteome in Dahl salt sensitive rats after 21 days of induction of hypertension, after 7 days and in control conditions.
Project description:Mlycd (malonyl-CoA decarboxylase) is a regulator of fatty acid metabolism. Lysine supplementation depletes kidney malonyl-CoA in hypertensive Dahl SS rats. As a key regulatory mechanism, lysine malonylation influences mitochondrial enzymes and fatty acid metabolism, with implications for CKD, hypertension, and other disorders. Yet how the balance between malonylation and acetylation is altered, and how this affects salt-sensitive hypertension, remains unclear. In this study, we examined the proteomic and metabolomic alterations resulting from Mlycd deficiency in Dahl salt-sensitive rats. This dataset contains proteomic profiles of heart, kidney, liver tissues as well as plasma and urine samples obtained from both Mlycd+/+ and Mlycd+/- animals.
Project description:Serum and glucocorticoid-induced kinase 1 (SGK1) activates the epithelial sodium channel (eNaC) in tubules. We examined renal SGK1 abundance in salt-adaptation and in salt-sensitive hypertension. Sprague-Dawley and Dahl salt-sensitive rats were placed on either 8% or 0.3% NaCl diets for 10 days. Plasma aldosterone levels were approximately 2.5-fold greater on 0.3% versus 8% NaCl diets in both rat strains. Both serum and glucocorticoid-induced kinase 1 transcript and protein abundance were less (P<0.01) in Sprague-Dawley rats and greater (P<0.01) in Dahl salt-sensitive rats on 8% versus 0.3% NaCl diets. The cDNA sequences of serum and glucocorticoid-induced kinase 1 in both strains of rat were the same. The present results provide evidence that the abundance of serum and glucocorticoid-induced kinase 1 in rat kidney may play a role in salt adaptation and the pathogenesis of hypertension and suggests that aldosterone is not the primary inducer of SGK1 in the Sprague-Dawley rat. Keywords = Rattus norvegicus, Sprague Dawley, Dahl SS/Jr, kidney, NaCl diet Keywords: other
Project description:Kidney injury mechanisms that develop in salt-sensitive (SS) hypertension are incompletely understood. Using the Dahl SS rat, which is a prominent model of salt-sensitive hypertension and associated kidney injury, loss of function of the pro-inflammatory transcription factor, ETS-1, corrects kidney microvascular autoregulatory dysfunction and injury. C-C motif chemokine ligand 2 (CCL2) is a direct target of ETS-1, so SS rats lacking Ccl2 (termed (SSCcl2 -/-) were therefore examined. Unlike SS rats, SSCcl2 -/- rats did not develop salt-sensitive hypertension, loss of autoregulation of afferent arterioles, or kidney injury. cDNA libraries from renal microvasculature of these rats was sequenced.
Project description:We perfomred sc RNA seq of intetinal immun cell and PBMCs to figure out the roles of intestine in development of salt-sensitive hypertension. We fed a high salt diet(4% NaCl) or a normal salt diet(0.2% NaCl) to Dahl-salt senstive rats for 4 weeks. We isolated immune cells from small instesinal lamin propria and blood.
