High-salt diet increases hormonal sensitivity in skin pre-capillary resistance vessels

2013 ◽  
Vol 207 (3) ◽  
pp. 577-581 ◽  
Author(s):  
F. Helle ◽  
T. V. Karlsen ◽  
O. Tenstad ◽  
J. Titze ◽  
H. Wiig
Keyword(s):  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Resistance Vessels ◽  
Capillary Resistance

Abstract P187: Nitric Oxide Function in Postural Tachycardia Syndrome During High and Low Sodium Diets

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Jorge E Celedonio ◽  
Victor C Nwazue ◽  
Emily M Garland ◽  
Cyndya A Shibao ◽  
Luis E Okamoto ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Healthy Subjects ◽  
High Salt ◽  
Postural Tachycardia Syndrome ◽  
Brachial Artery Diameter ◽  
High Salt Diet ◽  
Salt Diet ◽  
Postural Tachycardia ◽  
Resistance Vessels ◽  
Low Salt

Background: Postural tachycardia syndrome (POTS) is characterized by an increase in sympathetic activity, with an exaggerated rise in heart rate upon standing and symptoms of cerebral hypoperfusion. Endothelial/Nitric Oxide (NO) dysfunction might be involved in POTS pathophysiology. As part of the non-pharmacologic treatment of POTS, a high sodium diet is often recommended to increase plasma volume. We assessed endothelial/NO function in conduit vessels (using flow-mediated dilation, FMD) and resistance vessels (using finger pulse arterial tonometry, PAT) in POTS patients during high and low salt diets. Methods: In 14 female POTS patients (34±9 years, BMI 23±3 kg/m 2 ) and 13 matched healthy control subjects (29±4 years, BMI 24±3 kg/m 2 ), we evaluated the time course responses to FMD and PAT. Subjects were randomly assigned to either high salt diet (300mEq/day) or low salt diet (10mEq/day) for 6 days and crossed over to the other arm after 1 month. The areas under the curve for brachial artery diameter by FMD and finger artery dilation by PAT were compared between interventions and groups. Results: No differences in NO function in a conduit artery were seen. In contrast, in resistance vessels, high salt diet increased vasodilation in both POTS and healthy subjects (figure). In addition, POTS patients have greater vasodilation than healthy subjects during both low and high salt diets (p=0.036 and 0.033 for high and salt diets respectively). Conclusions: POTS patients may have an exaggerated NO response to reactive hyperemia in resistance vessels, but not in conductance vessels. This excessive vasodilation could contribute to POTS symptoms on standing.

463-P: Deterioration of Atherosclerosis via Dysbiosis in ApoE Null Mice Fed with High-Salt Diet

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 463-P
Author(s):  
TOMONORI KIMURA ◽  
YOSHITAKA HASHIMOTO ◽  
TAKAFUMI SENMARU ◽  
EMI USHIGOME ◽  
MASAHIDE HAMAGUCHI ◽  
...  
Keyword(s):  
High Salt ◽  
High Salt Diet ◽  
Salt Diet

scholarly journals Metabolic Syndrome and Salt-Sensitive Hypertension in Polygenic Obese TALLYHO/JngJ Mice: Role of Na/K-ATPase Signaling

2019 ◽  
Vol 20 (14) ◽  
pp. 3495 ◽  
Author(s):  
Yanling Yan ◽  
Jiayan Wang ◽  
Muhammad A. Chaudhry ◽  
Ying Nie ◽  
Shuyan Sun ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Significant Rise ◽  
Protein Carbonylation ◽  
High Salt ◽  
Kidney Cortex ◽  
High Salt Diet ◽  
Salt Diet ◽  
Salt Sensitive Hypertension

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.

scholarly journals High-Salt Diet Inhibits Expression of Angiotensin Type 2 Receptor in Resistance Arteries

Hypertension ◽  
2005 ◽  
Vol 45 (5) ◽  
pp. 853-859 ◽  
Author(s):  
Magdalena Gonzalez ◽  
Lorena Lobos ◽  
Felipe Castillo ◽  
Lorna Galleguillos ◽  
Nandy C. Lopez ◽  
...  
Keyword(s):  
High Salt ◽  
Resistance Arteries ◽  
High Salt Diet ◽  
Salt Diet ◽  
Angiotensin Type 2 Receptor ◽  
Angiotensin Type

Endothelin B receptors impair baroreflex function and increase blood pressure variability during high salt diet

2021 ◽  
pp. 102796
Author(s):  
Bryan K. Becker ◽  
Jermaine G. Johnston ◽  
Carolyn Young ◽  
Alfredo A. Torres Rodriguez ◽  
Chunhua Jin ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Variability ◽  
High Salt ◽  
Increase Blood Pressure ◽  
High Salt Diet ◽  
Salt Diet ◽  
Baroreflex Function ◽  
Endothelin B

Effect of a high-salt diet on oxidant enzyme activity in skeletal muscle microcirculation

2002 ◽  
Vol 282 (2) ◽  
pp. H395-H402 ◽  
Author(s):  
Deborah M. Lenda ◽  
Matthew A. Boegehold
Keyword(s):  
Skeletal Muscle ◽  
Xanthine Oxidase ◽  
Salt Intake ◽  
Normal Diet ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Arteriolar Wall ◽  
Xanthine Oxidase Inhibition ◽  
Alternate Source

Increased salt intake attenuates the endothelium-dependent dilation of skeletal muscle arterioles by abolishing local nitric oxide (NO) activity. There is evidence of oxidative stress in arteriolar and venular walls of rats fed a high-salt diet, and depressed arteriolar responses to acetylcholine (ACh) in these rats are reversed by scavengers of reactive oxygen species (ROS). In this study, we tested the hypothesis that this salt-dependent increase in microvascular ROS and the resulting attenuation of endothelium-dependent dilation are due to increased expression and/or activity of oxidant enzymes in the microvascular wall. Resting arteriolar and venular wall oxidant activity, as assessed by tetranitroblue tetrazolium reduction, was consistently higher in the spinotrapezius muscle of rats fed a high-salt diet (7% NaCl, HS) for 4–5 wk than in those fed a normal diet (0.45% NaCl, NS) for the same duration. Western analysis of protein from isolated microvessels showed no difference between HS and NS rats in the expression of NAD(P)H oxidase or xanthine oxidase. Inhibition of NAD(P)H oxidase and/or xanthine oxidase with diphenyleneiodonium chloride and oxypurinol, respectively, reduced resting arteriolar wall oxidant activity to normal levels in HS rats but had no effect in NS rats, suggesting that the basal activities of NAD(P)H oxidase and xanthine oxidase are increased in HS microvessels. However, inhibition of these enzymes in HS rats did not restore normal arteriolar responses to ACh, suggesting that this stimulus activates an alternate source of ROS that eliminates the role of NO in the subsequent dilation.

Overload proteinuria is followed by salt-sensitive hypertension caused by renal infiltration of immune cells

2002 ◽  
Vol 283 (5) ◽  
pp. F1132-F1141 ◽  
Author(s):  
Violeta Alvarez ◽  
Yasmir Quiroz ◽  
Mayerly Nava ◽  
Héctor Pons ◽  
Bernardo Rodríguez-Iturbe
Keyword(s):  
Interstitial Nephritis ◽  
Renal Damage ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Malondialdehyde Content ◽  
Induced Hypertension ◽  
Salt Sensitive Hypertension ◽  
And Control ◽  
And Oxidative Stress

Recent evidence suggests that salt-sensitive hypertension develops as a consequence of renal infiltration with immunocompetent cells. We investigated whether proteinuria, which is known to induce interstitial nephritis, causes salt-sensitive hypertension. Female Lewis rats received 2 g of BSA intraperitoneally daily for 2 wk. After protein overload (PO), 6 wk of a high-salt diet induced hypertension [systolic blood pressure (SBP) = 156 ± 11.8 mmHg], whereas rats that remained on a normal-salt diet and control rats (without PO) on a high-salt diet were normotensive. Administration of mycophenolate mofetil (20 mg · kg−1 · day−1) during PO resulted in prevention of proteinuria-related interstitial nephritis, reduction of renal angiotensin II-positive cells and oxidative stress (superoxide-positive cells and renal malondialdehyde content), and resistance to the hypertensive effect of the high-salt diet (SBP = 129 ± 12.2 mmHg). The present studies support the participation of renal inflammatory infiltrate in the pathogenesis of salt-sensitive hypertension and provide a direct link between two risk factors of progressive renal damage: proteinuria and hypertension.

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