Evaluation of Endothelial Function and Sympathetic Nervous Activity along the Glucose Continuum in Individuals with Habitual Low Sodium Intake

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 461-P
Author(s):  
SARA BAQAR ◽  
ELIF I. EKINCI
Keyword(s):  
Endothelial Function ◽  
Sodium Intake ◽  
Nervous Activity ◽  
Sympathetic Nervous Activity ◽  
Low Sodium ◽  
Sympathetic Nervous

scholarly journals Acute Alteration of Sympathetic Nervous Activity to Foot Shock Stress in SHR on Chronic Low Sodium Diet

1990 ◽  
Vol 31 (4) ◽  
pp. 552-552
Author(s):  
Yuji Naruse ◽  
Hiroshi Kawamura ◽  
Masahiro Maki ◽  
Hideaki Higashi ◽  
Kazuyoshi Tsukamoto ◽  
...  
Keyword(s):  
Nervous Activity ◽  
Sympathetic Nervous Activity ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Sympathetic Nervous ◽  
Shock Stress

scholarly journals Comparison of endothelial function and sympathetic nervous system activity along the glucose continuum in individuals with differing metabolic risk profiles and low dietary sodium intake

2019 ◽  
Vol 7 (1) ◽  
pp. e000606 ◽  
Author(s):  
Sara Baqar ◽  
Nora E Straznicky ◽  
Gavin Lambert ◽  
Yee Wen Kong ◽  
John B Dixon ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Heart Rate ◽  
Glucose Tolerance ◽  
Endothelial Function ◽  
Sodium Intake ◽  
Metabolic Risk ◽  
Low Sodium ◽  
Sympathetic Nervous

Objective: Low sodium intake may trigger sympathetic nervous system (SNS) activation and endothelial dysfunction. Studies have not explored these associations along the glucose continuum. Accordingly, we compared endothelial function and SNS activity in individuals with low sodium intake and differing categories of metabolic risk along the glucose continuum. We hypothesized that low sodium intake is associated with (1) impairment of endothelial function and (2) higher SNS activity in individuals with higher metabolic risk. Research Design and Methods: In this prospective observational study, participants (n=54) with low sodium intake (single 24 hours urine sodium excretion <150 mmol/24 hours) were categorized based on oral glucose tolerance testing as: normal glucose tolerance (NGT, n=10), impaired glucose tolerance (IGT, n=15), treatment naive type 2 diabetes (T2D−) (n=12) or treated type 2 diabetes (T2D+) (n=17). We assessed endothelial function using pulse amplitude tonometry (PAT) derived reactive hyperemic index and PAT ratio; arterial stiffness via augmentation index; muscle sympathetic nerve activity (MSNA) using microneurography; cardiac baroreflex; heart rate; blood pressure; glycosylated hemoglobin A1c (HbA1c) and lipid profile. Results: Mean (SD) sodium excretion was 110.6 (26) mmol/24 hours. Compared with NGT, IGT and T2D−, the T2D+ group had lower MSNA (p=0.005), PAT ratio (p=0.04) and baroreflex sensitivity (p=0.0002) and an augmented heart rate (p=0.02). The T2D+ group had appropriate mean (SD) glycemic (HbA1c 7.2 (1.72)%), total cholesterol (4.2 (1.0) mmol/L), low-density lipoprotein (2.2 (1.0) mmol/L) and blood pressure (systolic 136 (13), diastolic 78 (12)) (mm Hg) control. Conclusions: Individuals with T2D+ have impaired endothelial and baroreflex function, despite low sodium intake, appropriately managed cardiometabolic risk factors and lower SNS activity, compared with others along the glucose continuum. Whether low sodium intake is associated with modulation of the sympathovascular profile in T2D requires further investigation.

scholarly journals UBC-Nepal Expedition: acute alterations in sympathetic nervous activity do not influence brachial artery endothelial function at sea level and high altitude

2017 ◽  
Vol 123 (5) ◽  
pp. 1386-1396 ◽  
Author(s):  
Michael M. Tymko ◽  
Joshua C. Tremblay ◽  
Craig D. Steinback ◽  
Jonathan P. Moore ◽  
Alex B. Hansen ◽  
...  
Keyword(s):  
Endothelial Function ◽  
High Altitude ◽  
Sea Level ◽  
Brachial Artery ◽  
Nervous Activity ◽  
Sympathetic Nervous Activity ◽  
Positive Pressure ◽  
Lower Body ◽  
Saturation Pulse ◽  
Sympathetic Nervous

Evidence indicates that increases in sympathetic nervous activity (SNA), and acclimatization to high altitude (HA), may reduce endothelial function as assessed by brachial artery flow-mediated dilatation (FMD); however, it is unclear whether such changes in FMD are due to direct vascular constraint, or consequential altered hemodynamics (e.g., shear stress) associated with increased SNA as a consequence of exposure to HA. We hypothesized that 1) at rest, SNA would be elevated and FMD would be reduced at HA compared with sea-level (SL); and 2) at SL and HA, FMD would be reduced when SNA was acutely increased, and elevated when SNA was acutely decreased. Using a novel, randomized experimental design, brachial artery FMD was assessed at SL (344 m) and HA (5,050 m) in 14 participants during mild lower-body negative pressure (LBNP; −10 mmHg) and lower-body positive pressure (LBPP; +10 mmHg). Blood pressure (finger photoplethysmography), heart rate (electrocardiogram), oxygen saturation (pulse oximetry), and brachial artery blood flow and shear rate (Duplex ultrasound) were recorded during LBNP, control, and LBPP trials. Muscle SNA was recorded (via microneurography) in a subset of participants ( n = 5). Our findings were 1) at rest, SNA was elevated ( P < 0.01), and absolute FMD was reduced ( P = 0.024), but relative FMD remained unaltered ( P = 0.061), at HA compared with SL; and 2) despite significantly altering SNA with LBNP (+60.3 ± 25.5%) and LBPP (−37.2 ± 12.7%) ( P < 0.01), FMD was unaltered at SL ( P = 0.448) and HA ( P = 0.537). These data indicate that acute and mild changes in SNA do not directly influence brachial artery FMD at SL or HA. NEW & NOTEWORTHY The role of the sympathetic nervous system on endothelial function remains unclear. We used lower-body negative and positive pressure to manipulate sympathetic nervous activity at sea level and high altitude and measured brachial endothelial function via flow-mediated dilation. We found that acutely altering sympathetic nervous activity had no effect on endothelial function.

Sympathetic nervous activity in carriers of MC4R mutations

2006 ◽  
Vol 114 (S 1) ◽  
Author(s):  
D Heutling ◽  
F Sayk ◽  
C Dodt ◽  
HL Fehm ◽  
A Hinney ◽  
...  
Keyword(s):  
Nervous Activity ◽  
Sympathetic Nervous Activity ◽  
Sympathetic Nervous

Sympathetic nervous activity in patients with chronic renal failure

1994 ◽  
Vol 1 ◽  
pp. 314
Author(s):  
E. Gotoh ◽  
T. Matsukawa ◽  
S. Sumita ◽  
K. Ashino ◽  
N. Takagi ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Nervous Activity ◽  
Sympathetic Nervous Activity ◽  
Sympathetic Nervous

Variations in Individual Organ Release of Noradrenaline Measured by An Improved Radioenzymatic Technique; Limitations of Peripheral Venous Measurements in the Assessment of Sympathetic Nervous Activity

1981 ◽  
Vol 61 (5) ◽  
pp. 585-590 ◽  
Author(s):  
M. J. Brown ◽  
D. A. Jenner ◽  
D. J. Allison ◽  
C. T. Dollery
Keyword(s):  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Nervous Activity ◽  
Artery Stenosis ◽  
Plasma Noradrenaline ◽  
Sympathetic Nervous Activity ◽  
Release Of Noradrenaline ◽  
Noradrenaline Concentration ◽  
Sympathetic Nervous ◽  
Noradrenaline And Adrenaline

1. The validity of plasma noradrenaline as an index of sympathetic nervous activity was assessed by estimating variation in individual organ contribution to circulating concentrations. 2. Arteriovenous (A—V) differences in noradrenaline and adrenaline concentration were measured across several organs in nine patients with mild essential hypertension, in five with renal artery stenosis and 15 phaeochromocytoma patients. 3. In patients with phaeochromocytomas the percentage extraction of noradrenaline and adrenaline (estimated from the A—V differences) was similar across all organs, suggesting that adrenaline extraction could be used as a marker for noradrenaline extraction. 4. In the non-tumour patients the A—V difference for noradrenaline was less than that for adrenaline across most organs studied, reflecting the net result of noradrenaline release and extraction. The estimated contribution of various organs to the noradrenaline concentrations in their venous effluent was: heart. 21%; kidney 47%; legs 68%. 5. This pattern of A—V difference proved a positive diagnostic feature for non-tumour patients since it was not found even in the patients with small phaeochromocytomas, whose peripheral venous noradrenaline concentration alone did not distinguish them. 6. The venous-arterial difference across the adrenal glands of non-tumour patients was more than 10-fold greater for adrenaline than that for noradrenaline. Since the mean arterial concentration of noradrenaline was more than fivefold higher than that of adrenaline, the normal adrenal contribution to circulating noradrenaline is likely to be less than 2%. 7. In the patients with renal artery stenosis renal venous concentrations of noradrenaline (from the ischaemic kidney) were higher than arterial values, but mean arterial values were no higher than in the essential hypertensive patients. 8. Local variations in sympathetic activity may occur without altering the plasma noradrenaline concentration measured in peripheral plasma.

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