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High-salt Diet (high-salt + diet)
Selected AbstractsTime-Course and Mechanisms of Restored Vascular Relaxation by Reduced Salt Intake and Angiotensin II Infusion in Rats Fed a High-Salt DietMICROCIRCULATION, Issue 3 2009SCOTT T. MCEWEN ABSTRACT Objective: This study determined the mechanisms and time-course of recovery of vascular relaxation in middle cerebral arteries (MCAs) of salt-fed Sprague-Dawley rats returned to a low-salt (LS) diet (0.4% NaCl) or infused with low-dose angiotensin II (ANG II). Methods: Rats were fed a high-salt (HS) diet (4% NaCl) for 3 days or 4 weeks before returning to an LS diet for various periods. Other rats fed a HS diet (HS+ANG II) received a chronic (3 days) intravenous (i.v.) infusion of a low dose of ANG II (5 ng kg,1 min,1) to prevent salt-induced ANG II suppression. Results: The HS diet eliminated the increase in cerebral blood flow in response to acetylcholine (ACh) infusion and the relaxation of MCA in response to ACh, iloprost, cholera toxin, and reduced PO2. Recovery of vascular relaxation was slow, requiring at least 2 weeks of the LS diet, regardless of the duration of exposure to a HS diet. Hypoxic dilation was mediated by cyclo-oxygenase metabolites and ACh-induced dilation was mediated via nitric oxide in LS rats and in HS rats returned to the LS diet or receiving ANG II infusion. Conclusions: Returning to a LS diet for 2 weeks or chronic 3-day ANG II infusion restores the mechanisms that normally mediate cerebral vascular relaxation. [source] Decreased cortisol production in male type 1 diabetic patientsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 7 2003M. N. Kerstens Abstract Background It is unclear whether cortisol production and the 11,HSD-mediated cortisol to cortisone interconversion are different between type 1 diabetic patients and healthy subjects. Materials and methods Fourteen male, nonobese, normotensive type 1 diabetic patients without severe complications (HbA1c < 8·5%) were studied twice during a daily sodium intake of 50 and 200 mmol, and were then compared with 14 individually matched healthy subjects. Cortisol production was assessed by the sum of urinary cortisol metabolite excretion. Urinary ratios of (tetrahydrocortisol + allo-tetrahydrocortisol)/tetrahydro-cortisone [(THF + allo-THF)/THE] and of free cortisol/free cortisone [UFF/UFE] were determined as parameters of 11,HSD activity. Results Sum of urinary cortisol metabolite excretion during low- and high-salt diet was 7·4 ± 2·5 vs. 7·7 ± 2·3 nmol min,1 m,2 (NS) in diabetic patients and 9·7 ± 2·1 vs. 11·2 ± 4·1 nmol min,1 m,2 (NS) in healthy subjects, respectively (P < 0·05 vs. healthy subjects at both diets). The allo-THF excretion and allo-THF/THF ratios were lower in the diabetic than in the healthy males during both diets (P < 0·05). Urinary (THF + alloTHF)/THE and UFF/UFE were similar in both groups and remained unchanged after salt loading. Conclusions The sum of urinary cortisol metabolite excretion as a measure of cortisol production is lower in nonobese, normotensive type 1 diabetic males with adequate glycaemic control and without severe complications, irrespective of sodium intake. We suggest that this is at least in part as result of diminished 5, reductase activity, resulting in a decreased cortisol metabolic clearance. In type 1 diabetic and in healthy males, the 11,HSD setpoint is not affected by physiological variations in sodium intake. [source] Region-specific changes in sympathetic nerve activity in angiotensin II,salt hypertension in the ratEXPERIMENTAL PHYSIOLOGY, Issue 1 2010John W. Osborn It is now well accepted that many forms of experimental hypertension and human essential hypertension are caused by increased activity of the sympathetic nervous system. However, the role of region-specific changes in sympathetic nerve activity (SNA) in the pathogenesis of hypertension has been difficult to determine because methods for chronic measurement of SNA in conscious animals have not been available. We have recently combined indirect, and continuous and chronic direct, assessment of region-specific SNA to characterize hypertension produced by administration of angiotensin II (Ang II) to rats consuming a high-salt diet (Ang II,salt hypertension). Angiotensin II increases whole-body noradrenaline (NA) spillover and depressor responses to ganglionic blockade in rats consuming a high-salt diet, but not in rats on a normal-salt diet. Despite this evidence for increased ,whole-body SNA' in Ang II,salt hypertensive rats, renal SNA is decreased in this model and renal denervation does not attenuate the steady-state level of arterial pressure. In addition, neither lumbar SNA, which largely targets skeletal muscle, nor hindlimb NA spillover is changed from control levels in Ang II,salt hypertensive rats. However, surgical denervation of the splanchnic vascular bed attenuates/abolishes the increase in arterial pressure and total peripheral resistance, as well as the decrease in vascular capacitance, observed in Ang II,salt hypertensive rats. We hypothesize that the ,sympathetic signature' of Ang II,salt hypertension is characterized by increased splanchnic SNA, no change in skeletal muscle SNA and decreased renal SNA, and this sympathetic signature creates unique haemodynamic changes capable of producing sustained hypertension. [source] Survival of sea-water-adapted trout, Salmo trutta L. ranched in a Danish fjordFISHERIES MANAGEMENT & ECOLOGY, Issue 4 2000S. S. Pedersen The effect of seawater adaptation on the survival of coastally released post-smolt trout, Salmo trutta L., was investigated by release: (1) directly (with no adaptation); (2) after retention in net pens in the sea for 29,131 days (delayed release); (3) after feeding with a high-salt diet (12,13.5% NaCl) for 4 weeks; and (4) after a combination of (2) and (3). In total, 17 640 trout (age = 1+, 1.5 and 2+ years; mean fork lengths = 18.2,25.6 cm) were released in 14 batches in the summer or autumn months of 1986,1989. All fish were of domesticated origin and Carlin tagged. Survival and instantaneous mortality rates (total and fishing mortality) were estimated from reported recaptures. Mortality rates were estimated for: (1) the post-smolt period; (2) the period until the legal size of capture (40 cm) was attained; and (3) for larger sea-trout. Release with a delay of 4 weeks gave an increased survival rate. A longer adaptation period did not increase survival. On average, survival was increased by 36%. Survival was not increased by high-salt diets. Until attainment of the legal size for capture, survival was 9.6% higher on average, with extremes as low as 1.7% and as high as 38% in individual batches. [source] Angiotensin II Is a Critical Mediator of Prazosin-Induced Angiogenesis in Skeletal MuscleMICROCIRCULATION, Issue 6 2007Matthew C. Petersen ABSTRACT Objective: The purpose of this study was to determine whether a high-salt diet modulates physiological angiogenesis in skeletal muscle by altering angiotensin II (ANGII) and vascular endothelial growth factor (VEGF) levels. Methods: Sprague-Dawley rats were placed on a control diet (0.4% NaCl by weight) or high-salt diet (4.0% NaCl) prior to treatment with the vasodilator prazosin in the drinking water. In addition, a group of animals fed high salt were infused intravenously with ANGII at a low dose to prevent ANGII suppression by high salt, and a group of rats fed control diet were treated with the angiotensin II type I (AT1) receptor blocker losartan and prazosin. Results: Prazosin induced significant angiogenesis in the tibialis anterior muscle after 1 week of treatment. High-salt-fed rats demonstrated a complete inhibition of this angiogenic response. Maintenance of ANGII levels restored prazosin-induced angiogenesis in animals fed a high-salt diet. In addition, losartan treatment blocked prazosin-induced angiogenesis in animals on a control diet. Western blot analysis indicated that prazosin-induced angiogenesis was independent of changes in muscle levels of VEGF. Conclusions: This study demonstrates an inhibitory effect of high salt intake on prazosin-induced angiogenesis. Further, these results indicate that ANGII acting through the AT1 receptor is a critical pathway in this model of angiogenesis. [source] Survival of sea-water-adapted trout, Salmo trutta L. ranched in a Danish fjordFISHERIES MANAGEMENT & ECOLOGY, Issue 4 2000S. S. Pedersen The effect of seawater adaptation on the survival of coastally released post-smolt trout, Salmo trutta L., was investigated by release: (1) directly (with no adaptation); (2) after retention in net pens in the sea for 29,131 days (delayed release); (3) after feeding with a high-salt diet (12,13.5% NaCl) for 4 weeks; and (4) after a combination of (2) and (3). In total, 17 640 trout (age = 1+, 1.5 and 2+ years; mean fork lengths = 18.2,25.6 cm) were released in 14 batches in the summer or autumn months of 1986,1989. All fish were of domesticated origin and Carlin tagged. Survival and instantaneous mortality rates (total and fishing mortality) were estimated from reported recaptures. Mortality rates were estimated for: (1) the post-smolt period; (2) the period until the legal size of capture (40 cm) was attained; and (3) for larger sea-trout. Release with a delay of 4 weeks gave an increased survival rate. A longer adaptation period did not increase survival. On average, survival was increased by 36%. Survival was not increased by high-salt diets. Until attainment of the legal size for capture, survival was 9.6% higher on average, with extremes as low as 1.7% and as high as 38% in individual batches. [source] The Salt-Inducible Kinase, SIK, Is Induced by Depolarization in BrainJOURNAL OF NEUROCHEMISTRY, Issue 6 2000Jonathan D. Feldman Abstract: Membrane depolarization of neurons is thought to lead to changes in gene expression that modulate neuronal plasticity. We used representational difference analysis to identify a group of cDNAs that are induced by membrane depolarization or by forskolin, but not by neurotrophins or growth factors, in PC12 pheochromocytoma cells. One of these genes, SIK (salt- inducible kinase), is a member of the sucrose-nonfermenting 1 protein kinase/AMP-activated protein kinase protein kinase family that was also recently identified from the adrenal gland of rats treated with high-salt diets. SIK mRNA is induced up to eightfold in specific regions of the hippocampus and cortex in rats, following systemic kainic acid administration and seizure induction. [source] | |||||||||||||