Disease relevance of Rats, Inbred Dahl

• Together with the induction of salt-dependent hypertension in genetically salt-resistant Dahl rats by D(3) receptor blockade, the data strongly suggest that the deficiency in dopamine D(3) receptors represents an important pathophysiological factor in the development of salt-dependent hypertension [1].
• We conclude that high salt intake in salt-sensitive hypertensive Dahl rats produces hypertension, cardiac hypertrophy, and heterologous desensitization of cardiac adenylyl cyclase [2].
• We tested whether these abnormalities influenced the ability of conscious prehypertensive Dahl salt-sensitive rats to excrete a moderate intravenous isotonic saline volume load (0.9% NaCl, 3% body weight i.v.). During control, 30-minute volume expansion, and 2-hour recovery periods, arterial blood pressure and heart rate did not change [3].
• Influence of cadmium on two-kidney Goldblatt hypertension in Dahl rats [4].
• Involvement of angiotensin II in development of spontaneous nephrosis in Dahl salt-sensitive rats [5].

Psychiatry related information on Rats, Inbred Dahl

• The influence of the renin gene on alcohol consumption in Dahl rats [6].

High impact information on Rats, Inbred Dahl

• Brain "ouabain" mediates the sympathoexcitatory and hypertensive effects of high sodium intake in Dahl salt-sensitive rats [7].
• To examine the central and efferent portions of the baroreflex arc, we electrically stimulated the aortic depressor nerve of urethane anesthetized Dahl salt-sensitive and Dahl salt-resistant rats while recording arterial pressure, heart rate, and sympathetic nerve activity [8].
• Genome scan and congenic strains for blood pressure QTL using Dahl salt-sensitive rats [9].
• The SOD mimetic tempol ameliorates glomerular injury and reduces mitogen-activated protein kinase activity in Dahl salt-sensitive rats [10].
• In summary, both expression and function of the renal dopamine D(3) receptor are impaired in salt-sensitive Dahl rats [1].

Chemical compound and disease context of Rats, Inbred Dahl

• Renal intramedullary infusion of L-arginine prevents reduction of medullary blood flow and hypertension in Dahl salt-sensitive rats [11].
• Clofibrate prevents the development of hypertension in Dahl salt-sensitive rats [12].
• Role of epinephrine in the development of hypertension in Dahl salt-sensitive rats [13].
• Taurine amplifies renal kallikrein and prevents salt-induced hypertension in Dahl rats [14].
• In contrast, the diphenylhexatriene anisotropy, which is related to the core membrane microviscosity, was significantly reduced in the Dahl salt-sensitive rats (irrespective of salt intake level) and in the Sabra hypertension-prone rats with developed salt hypertension [15].

Biological context of Rats, Inbred Dahl

• These structural studies provide a basis for genetic investigation into the relationship of the renin gene to blood pressure in Dahl rats [16].
• L-arginine administration normalizes pressure natriuresis in hypertensive Dahl rats [17].
• Brain 'ouabain' and desensitization of arterial baroreflex by high sodium in Dahl salt-sensitive rats [18].
• Angiotensin II-induced phosphorylation of proteins was examined in isolated myocytes from hearts of Dahl rats [19].
• OBJECTIVE: The present study aimed to characterize the influence of salt intake on the gene expression of the kidney specific chloride channels CLC-K1 and CLC-K2 in the kidneys of salt-resistant and salt-sensitive Dahl rats [20].

Anatomical context of Rats, Inbred Dahl

• This study examined the effect of 25% deuterium oxide in drinking water on systolic blood pressure, uptakes of calcium, and rubidium 86 by aortas of Dahl salt-sensitive rats on 0.4% (low) and 8% (high) sodium chloride (salt) diet [21].
• In membranes from Dahl salt-sensitive rats on a high-salt diet (8%) basal, isoproterenol-, 5'-guanylylimidodiphosphate-, and forskolin-stimulated adenylyl cyclase was reduced compared with the low-salt (0.4%) group and Dahl salt-resistant rats on either 0.4% or 8% sodium chloride [2].
• Enhanced chloride reabsorption in the loop of Henle in Dahl salt-sensitive rats [22].
• We evaluated the mechanical properties of the carotid artery in anesthetized Dahl rats with or without long-term treatment with the diuretic compound indapamide [23].
• Plasma glucose, insulin, and triglyceride concentration, blood pressure, and insulin action on isolated adipocytes were determined in weight-matched Sprague-Dawley, Dahl salt-resistant, and Dahl salt-sensitive rats [24].

Associations of Rats, Inbred Dahl with chemical compounds

• Dahl salt-sensitive rats (n = 6 per group) on standard or salt-enriched chow were treated for 8 wk with O (36 +/- 4 mg/kg per d), C (94 +/- 2 mg/kg per d), or placebo [25].
• METHODS: Dahl salt-sensitive rats fed a high-salt diet for seven weeks were divided into three groups: eight untreated rats (DHF group), eight rats given high-dose amlodipine (10 mg/kg/day; HDA group) and seven rats given low-dose amlodipine (1 mg/kg/day; LDA group) [26].
• Salt-sensitive (DS) and salt-resistant (DR) Dahl rats were treated for 8 wk with high salt diet (4% NaCl) alone or in combination with the ET(A) receptor antagonist LU135252 (60 mg/kg per d) [27].
• To test this hypothesis in Dahl salt-sensitive rats given sodium chloride (4%) for 3 weeks, we supplemented dietary potassium (2.1%) with either KCl (n = 16) or KHCO3 (n = 16) [28].
• Failure of salt loading to inhibit tissue norepinephrine turnover in prehypertensive Dahl salt-sensitive rats [29].

Gene context of Rats, Inbred Dahl

• Effects of AT1 receptor blockade on renal injury and mitogen-activated protein activity in Dahl salt-sensitive rats [30].
• Marked reduction of mortality in salt-loaded Dahl salt-sensitive rats by the new, selective endothelin ETA receptor antagonist, J-105859 [31].
• Within the kidney, nNOS mRNA levels were significantly decreased in salt-sensitive Dahl rats compared with those in salt-resistant Dahl rats, in cortex, outer and inner medulla (50, 40 and 30%, respectively) under all dietary conditions [32].
• Decreased expression of arginase II in the kidneys of Dahl salt-sensitive rats [33].
• The expression levels of kallikrein 1 protein were also suppressed in Dahl salt-sensitive rats compared with those in Lewis rats [34].

Analytical, diagnostic and therapeutic context of Rats, Inbred Dahl

• The membrane fractions from vas deferens of salt-sensitive Dahl rats on the high-salt diet, on the other hand, showed decreased ATP-dependent Ca2+ transport compared to those from salt-sensitive Dahl rats on the low-salt diet [35].
• Imidapril (DSHF-IM, n = 8, 1 mg/kg/day, subdepressor dose) or vehicle (DSHF-V, n = 8) was given from stage DSLVH to DSHF for 7 weeks, and age-matched (18 weeks) Dahl salt-resistant rats fed the same diet served as the control group (DR-C, n = 8) [36].
• Using real-time PCR, we found calpain 6 and 9 down-regulated by more than 50% and the endogenous calpain inhibitor calpastatin up-regulated by 225%, respectively, in the hearts of Dahl salt-sensitive rats on a high salt (4% NaCl) compared to normal salt diet [37].
• Probucol suppresses the development of chronic renal failure in Dahl salt-sensitive rats: an animal model of spontaneous focal and segmental glomerulosclerosis [38].
• Northern blot analysis revealed an increase in the steady state mRNA levels of fibronectin, an important component of mesangial matrices, in the renal cortex, but not in the renal medulla, only in salt-loaded Dahl salt-sensitive rats [39].

References