scholarly journals Effect of high-salt diet on blood pressure and body fluid composition in patients with type 1 diabetes: randomized controlled intervention trial

2020 ◽  
Vol 8 (1) ◽  
pp. e001039
Author(s):  
Eliane F E Wenstedt ◽  
Nienke M G Rorije ◽  
Rik H G Olde Engberink ◽  
Kim M van der Molen ◽  
Youssef Chahid ◽  
...  

IntroductionPatients with type 1 diabetes are susceptible to hypertension, possibly resulting from increased salt sensitivity and accompanied changes in body fluid composition. We examined the effect of a high-salt diet (HSD) in type 1 diabetes on hemodynamics, including blood pressure (BP) and body fluid composition.Research design and methodsWe studied eight male patients with type 1 diabetes and 12 matched healthy controls with normal BP, body mass index, and renal function. All subjects adhered to a low-salt diet and HSD for eight days in randomized order. On day 8 of each diet, extracellular fluid volume (ECFV) and plasma volume were calculated with the use of iohexol and 125I-albumin distribution. Hemodynamic measurements included BP, cardiac output (CO), and systemic vascular resistance.ResultsAfter HSD, patients with type 1 diabetes showed a BP increase (mean arterial pressure: 85 (5) mm Hg vs 80 (3) mm Hg; p<0.05), while BP in controls did not rise (78 (5) mm Hg vs 78 (5) mm Hg). Plasma volume increased after HSD in patients with type 1 diabetes (p<0.05) and not in controls (p=0.23). There was no significant difference in ECFV between diets, while HSD significantly increased CO, heart rate (HR) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) in type 1 diabetes but not in controls. There were no significant differences in systemic vascular resistance, although there was a trend towards an HSD-induced decrease in controls (p=0.09).ConclusionsIn the present study, patients with type 1 diabetes show a salt-sensitive BP rise to HSD, which is accompanied by significant increases in plasma volume, CO, HR, and NT-proBNP. Underlying mechanisms for these responses need further research in order to unravel the increased susceptibility to hypertension and cardiovascular disease in diabetes.Trial registration numbersNTR4095 and NTR4788.

1985 ◽  
Vol 249 (3) ◽  
pp. H577-H584
Author(s):  
A. P. Rocchini ◽  
K. P. Gallagher ◽  
M. J. Botham ◽  
J. H. Lemmer ◽  
C. A. Szpunar ◽  
...  

The ability of a chronic high-salt diet to prevent fatal hemorrhagic shock was examined in 36 mongrel dogs. Twenty-one dogs received a dietary supplement of 9 g sodium chloride/day for 6 wk, and 15 dogs received the same basic diet for 6 wk but without the sodium chloride supplement. Hemorrhagic shock was induced in all dogs by bleeding into an overhanging sealed reservoir. After 3 h of shock, salt-pretreated dogs had a lower systemic vascular resistance of 0.70 +/- 0.02 versus 1.44 +/- 0.04 mmHg X ml-1 X min X kg (P less than 0.01) and a higher cardiac output of 53 +/- 3 versus 26 +/- 3 ml X min-1 X kg-1 (P less than 0.01) than was observed in controls. At 2.5 h of shock, the salt-pretreated dogs also experienced an increase in gastrointestinal (P less than 0.01), hepatic arterial, (P less than 0.05), kidney (P less than 0.05), brain (P less than 0.01), and heart blood flows (P less than 0.001) compared with 0.5 h of shock, whereas the control dogs experienced no increased flow during this same period. We also observed that after 3 h of hypotension there was a significantly smaller increase in plasma renin activity in the salt-pretreated dogs. Administration of 0.1 U X kg-1 X min-1 of hog renin eliminated the differences in systemic vascular resistance, cardiac output, and survival in five salt-pretreated dogs.


Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Tengis S Pavlov ◽  
Daria V Ilatovskaya ◽  
Gregory Blass ◽  
Oleg Palygin ◽  
Vladislav Levchenko ◽  
...  

Dahl salt sensitive (SS) rat is a well-established model for studying salt-induced hypertension and associated kidney injury. We and others have previously shown that salt-sensitive hypertension is accompanied by increased renal production of reactive oxygen species (ROS) and excessive activity of ENaC in the distal nephron. To investigate role of ROS, and specifically NADPH oxidase 4 (Nox4), a primary source of ROS in the kidney, involved in the regulation of ENaC activity during the development of SS hypertension and type 1 diabetes, we performed patch clamp analysis in the cortical collecting ducts of Dahl SS rats and SS rats lacking Nox4 (Nox4 -/- ). We found that SS rats fed a 4% NaCl diet have significantly elevated ENaC activity even 3 days post diet change. ENaC activity (NP o ) was 0.57±0.08, 1.32±0.3 and 1.69±0.06 before, 3 days and 3 weeks after high salt diet, respectively. In contrast, ENaC activity was not significantly different in SS Nox4-/- animals after high salt diet. To study the role of Nox4 in hyperglycemic conditions, diabetes was induced in 6 weeks old male wild type or Nox4 -/- rats with a single i.p. injection of STZ. We found that ENaC activity in the animals that were hyperglycemic for 11 weeks was elevated compared to control rats (0.71±0.10 and 1.27±0.2; p<0.05) and this effect was mediated via changes in channel open probability. Nox4 deficiency blunts the effect of hyperglycemia on ENaC activity (in STZ-treated animals open probability significantly increased from 0.43±0.06 to 0.86±0.07 in WT rats, but in the Nox4 -/- group did not change: P o was 0.51±0.06 and 0.51±0.07, respectively) that delineates the importance of Nox4-mediated ROS production for regulation of ENaC open probability. Taken together, our data indicate that ENaC activity in Dahl SS rats is elevated following a change of salt diet (3 days and 3 weeks at high salt) and after the development of type 1 diabetes. Furthermore, Nox4 plays a crucial role in these effects of high salt and hyperglycemia on ENaC activity.


2014 ◽  
Author(s):  
Francisco Javier Vilchez-Lopez ◽  
Isabel Mateo-Gavira ◽  
Florentino Carral-San Laureano ◽  
Maria Victoria Garcia-Palacios ◽  
Jose Ortego-Rojo ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Michal Kulecki ◽  
Dariusz Naskret ◽  
Mikolaj Kaminski ◽  
Dominika Kasprzak ◽  
Pawel Lachowski ◽  
...  

AbstractThe non-dipping pattern is nighttime systolic blood pressure (SBP) fall of less than 10%. Several studies showed that the non-dipping pattern, increased mean platelet volume (MPV), and platelet distribution width (PDW) are associated with elevated cardiovascular risk. Hypertensives with the non-dipping pattern have higher MPV than the dippers but this relationship was never investigated among people with type 1 diabetes mellitus (T1DM). This study aimed to investigate the association between the central dipping pattern and platelet morphology in T1DM subjects. We measured the central and brachial blood pressure with a validated non-invasive brachial oscillometric device—Arteriograph 24—during twenty-four-hour analysis in T1DM subjects without diagnosed hypertension. The group was divided based on the central dipping pattern for the dippers and the non-dippers. From a total of 62 subjects (32 males) aged 30.1 (25.7–37) years with T1DM duration 15.0 (9.0–20) years, 36 were non-dippers. The non-dipper group had significantly higher MPV (MPV (10.8 [10.3–11.5] vs 10.4 [10.0–10.7] fl; p = 0.041) and PDW (13.2 [11.7–14.9] vs 12.3 [11.7–12.8] fl; p = 0.029) than dipper group. Multivariable logistic regression revealed that MPV (OR 3.74; 95% CI 1.48–9.45; p = 0.005) and PDW (OR 1.91; 95% CI 1.22–3.00; p = 0.005) were positively associated with central non-dipping pattern adjusting for age, sex, smoking status, daily insulin intake, and height. MPV and PDW are positively associated with the central non-dipping pattern among people with T1DM.


2019 ◽  
Vol 20 (14) ◽  
pp. 3495 ◽  
Author(s):  
Yanling Yan ◽  
Jiayan Wang ◽  
Muhammad A. Chaudhry ◽  
Ying Nie ◽  
Shuyan Sun ◽  
...  

We have demonstrated that Na/K-ATPase acts as a receptor for reactive oxygen species (ROS), regulating renal Na+ handling and blood pressure. TALLYHO/JngJ (TH) mice are believed to mimic the state of obesity in humans with a polygenic background of type 2 diabetes. This present work is to investigate the role of Na/K-ATPase signaling in TH mice, focusing on susceptibility to hypertension due to chronic excess salt ingestion. Age-matched male TH and the control C57BL/6J (B6) mice were fed either normal diet or high salt diet (HS: 2, 4, and 8% NaCl) to construct the renal function curve. Na/K-ATPase signaling including c-Src and ERK1/2 phosphorylation, as well as protein carbonylation (a commonly used marker for enhanced ROS production), were assessed in the kidney cortex tissues by Western blot. Urinary and plasma Na+ levels were measured by flame photometry. When compared to B6 mice, TH mice developed salt-sensitive hypertension and responded to a high salt diet with a significant rise in systolic blood pressure indicative of a blunted pressure-natriuresis relationship. These findings were evidenced by a decrease in total and fractional Na+ excretion and a right-shifted renal function curve with a reduced slope. This salt-sensitive hypertension correlated with changes in the Na/K-ATPase signaling. Specifically, Na/K-ATPase signaling was not able to be stimulated by HS due to the activated baseline protein carbonylation, phosphorylation of c-Src and ERK1/2. These findings support the emerging view that Na/K-ATPase signaling contributes to metabolic disease and suggest that malfunction of the Na/K-ATPase signaling may promote the development of salt-sensitive hypertension in obesity. The increased basal level of renal Na/K-ATPase-dependent redox signaling may be responsible for the development of salt-sensitive hypertension in polygenic obese TH mice.


2021 ◽  
pp. 102796
Author(s):  
Bryan K. Becker ◽  
Jermaine G. Johnston ◽  
Carolyn Young ◽  
Alfredo A. Torres Rodriguez ◽  
Chunhua Jin ◽  
...  

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