Effect of Indomethacin on Blood Pressure in the Normotensive Unanaesthetized Rabbit: Possible Relation to Prostaglandin Synthesis Inhibition

1979 ◽  
Vol 57 (4) ◽  
pp. 359-365 ◽  
Author(s):  
J. Colina-Chourio ◽  
J. C. McGiff ◽  
A. Nasjletti
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Control Period ◽  
Urine Volume ◽  
Urinary Sodium Excretion ◽  
Prostaglandin Synthesis ◽  
Endogenous Prostaglandins ◽  
Cumulative Difference ◽  
Aortic Blood Pressure ◽  
Regulation Of Blood Pressure

1. To test the hypothesis that endogenous prostaglandins contribute to the regulation of blood pressure, we studied the effect of an inhibitor of prostaglandin synthesis, indomethacin, on mean aortic blood pressure in the normotensive, unanaesthetized rabbit. 2. Daily administration of indomethacin at 42 μmol/kg subcutaneously, but not of vehicle only, for 14 consecutive days, elevated the average mean arterial pressure in seven rabbits from 88 ± 3 mmHg on the last day of the control period to 105 + 3 mmHg (P < 0·01) and 107 ± 2 mmHg (P < 0·01) on days 6 and 14 of indomethacin treatment respectively, and reduced the urinary excretion of prostaglandin-like substance from 1·06 ± 0·26 to 0·17 ± 0·05 nmol of prostaglandin E2 equivalents/ day (P < 0·05; n = 5). Neither indomethacin nor the vehicle affected the intake of water, the 24 h urine volume, the cumulative difference between sodium intake and urinary sodium excretion, or the plasma volume. 3. The results of the study are compatible with the hypothesis that one or more prostaglandins contribute to maintain normotension in the rabbit and that reduction in prostaglandin biosynthesis may cause blood pressure to rise.

scholarly journals Association between 24-h urinary sodium and potassium excretion and blood pressure among Chinese adults aged 18–69 years

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiaofu Du ◽  
Le Fang ◽  
Jianwei Xu ◽  
Xiangyu Chen ◽  
Yamin Bai ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Inverse Association ◽  
Potassium Excretion ◽  
Chinese Adults ◽  
Potassium Intake ◽  
Sodium And Potassium

AbstractThe direction and magnitude of the association between sodium and potassium excretion and blood pressure (BP) may differ depending on the characteristics of the study participant or the intake assessment method. Our objective was to assess the relationship between BP, hypertension and 24-h urinary sodium and potassium excretion among Chinese adults. A total of 1424 provincially representative Chinese residents aged 18 to 69 years participated in a cross-sectional survey in 2017 that included demographic data, physical measurements and 24-h urine collection. In this study, the average 24-h urinary sodium and potassium excretion and sodium-to-potassium ratio were 3811.4 mg/day, 1449.3 mg/day, and 4.9, respectively. After multivariable adjustment, each 1000 mg difference in 24-h urinary sodium excretion was significantly associated with systolic BP (0.64 mm Hg; 95% confidence interval [CI] 0.05–1.24) and diastolic BP (0.45 mm Hg; 95% CI 0.08–0.81), and each 1000 mg difference in 24-h urinary potassium excretion was inversely associated with systolic BP (− 3.07 mm Hg; 95% CI − 4.57 to − 1.57) and diastolic BP (− 0.94 mm Hg; 95% CI − 1.87 to − 0.02). The sodium-to-potassium ratio was significantly associated with systolic BP (0.78 mm Hg; 95% CI 0.42–1.13) and diastolic BP (0.31 mm Hg; 95% CI 0.10–0.53) per 1-unit increase. These associations were mainly driven by the hypertensive group. Those with a sodium intake above about 4900 mg/24 h or with a potassium intake below about 1000 mg/24 h had a higher risk of hypertension. At higher but not lower levels of 24-h urinary sodium excretion, potassium can better blunt the sodium-BP relationship. The adjusted odds ratios (ORs) of hypertension in the highest quartile compared with the lowest quartile of excretion were 0.54 (95% CI 0.35–0.84) for potassium and 1.71 (95% CI 1.16–2.51) for the sodium-to-potassium ratio, while the corresponding OR for sodium was not significant (OR, 1.28; 95% CI 0.83–1.98). Our results showed that the sodium intake was significantly associated with BP among hypertensive patients and the inverse association between potassium intake and BP was stronger and involved a larger fraction of the population, especially those with a potassium intake below 1000 mg/24 h should probably increase their potassium intake.

Abstract P276: A High Sodium Diet Reduces Cutaneous Microvascular Function In Normotensive Individuals With Salt Sensitive Blood Pressure

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Jordan C Patik ◽  
Joseph M Stock ◽  
Nathan T Romberger ◽  
Shannon L Lennon ◽  
William B Farquhar ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Function ◽  
Sodium Intake ◽  
Local Heating ◽  
Urinary Sodium Excretion ◽  
Microvascular Function ◽  
Dietary Sodium ◽  
Heating Unit ◽  
Doppler Flowmetry ◽  
High Sodium

Impaired vascular function likely contributes to the association between dietary sodium intake and the development of cardiovascular disease. Using the cutaneous microvasculature as a model, we have previously shown that a high sodium (HS) diet blunts local heating-induced vasodilation in normotensive individuals with salt resistant (SR) blood pressure (BP). However, the effect of a HS diet on the cutaneous microvasculature in normotensive salt sensitive (SS) individuals remains unclear. Therefore, we tested the hypothesis that cutaneous microvascular function is reduced by a HS diet to a greater degree in SS compared to SR individuals. After each 7-day controlled feeding diet (low sodium (LS) = 20 mmol/day; HS = 300 mmol/day), an intradermal microdialysis fiber was inserted in the ventral forearm and perfused with Ringer’s solution. Skin blood flow (SkBF) was continuously monitored via laser Doppler flowmetry and a local heating unit was placed over the fiber and heated to 42°C until SkBF reached a stable plateau. Site-specific maximal SkBF was determined by perfusing 28mM sodium nitroprusside and heating to 43°C. Mean arterial pressure (MAP) was assessed at regular intervals on the contralateral arm and was used to calculate cutaneous vascular conductance (CVC = SkBF / MAP). Subjects wore a 24-hr ambulatory BP monitor and collected their urine on the final day of each diet. Fourteen subjects (9W / 5M, 42 ± 14 yr) whose MAP increased >5 mmHg (Δ8 ± 1 mmHg) on the HS diet were defined as SS and were compared to 14 age- (43± 14 yr) and sex-matched SR subjects (Δ1 ± 3 mmHg). SS and SR had similar MAP at baseline (88 ± 9 vs. 90 ± 8 mmHg, P = 0.88) and urinary sodium excretion was increased similarly across groups by the HS diet (Δ239 ± 104 vs. Δ220 ± 66 mmol / 24 hr, P = 0.20). Cutaneous vasodilation in response to local heating was decreased on the HS diet relative to the LS diet in both SS (Δ-9 ± 9 %CVCmax, P = 0.005) and SR (Δ-9 ± 9 %CVCmax, P=0.005); however, there was not a group x diet interaction (P = 0.99). In contrast to our hypothesis, these results suggest that the deleterious effects of high sodium diets on cutaneous microvascular function are similar in normotensive salt sensitive and salt resistant individuals.

Comparison of fast and slow pressor effects of angiotensin II in the conscious rat

1981 ◽  
Vol 241 (3) ◽  
pp. H381-H388 ◽  
Author(s):  
A. J. Brown ◽  
J. Casals-Stenzel ◽  
S. Gofford ◽  
A. F. Lever ◽  
J. J. Morton
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Control Period ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Pressor Effect ◽  
Ang Ii ◽  
Conscious Rat ◽  
Female Wistar Rats

Female Wistar rats were infused intravenously with 5% dextrose for 3 days, then with angiotensin II (ANG II) in 5% dextrose at 20 ng . kg-1 . min-1 for 7 days, and finally with dextrose for 2.5 days. ANG II raised mean arterial pressure (MAP) gradually; by the 7th day it was 49.7 mmHg higher than during the dextrose control period in the same rats. Control rats were infused with dextrose for 12.5 days; MAP did not change. Plasma ANG II concentration was measured during infusion. In hypertensive rats on the 7th day of ANG II infusion, it was six times higher than in control rats infused with dextrose. Changes of blood pressure and plasma ANG II concentration were compared in further rats infused with much larger doses of ANG II. Rats receiving 270 ng . kg-1 . min-1 for 1 h had an almost maximal direct pressor response, MAP rising 45.3 mmHg and plasma ANG II rising 32-fold compared with controls. Thus, infusion of ANG II at low dose without direct pressor effect gradually raises blood pressure to a level similar to the maximum direct pressor effect produced by larger doses of ANG II. Sodium balance and food and water intakes were also measured and did not change during prolonged infusion of ANG II at 20 ng . kg-1 . min-1. Thus, the slow pressure effect of ANG II develops at a lower and more nearly physiological plasma concentration of the peptide than do the direct pressor effect and the effects on drinking, eating, and urinary sodium excretion.

Steady-state arterial pressure-urinary output relationships during ovine pregnancy

1992 ◽  
Vol 263 (5) ◽  
pp. R1141-R1146
Author(s):  
E. W. Quillen ◽  
B. S. Nuwayhid
Keyword(s):  
Renal Function ◽  
Steady State ◽  
Arterial Pressure ◽  
Sodium Intake ◽  
Control Level ◽  
Urine Volume ◽  
Urinary Sodium Excretion ◽  
Pregnant Sheep ◽  
Plasma Angiotensin ◽  
Steady State Levels

To determine the effects of long-term changes in sodium intake on mean arterial pressure (MAP) regulation during pregnancy, nonpregnant (n = 16) and 110- to 140-day pregnant (n = 13) ewes received total daily sodium intakes of 10, 30, 100, 400, and 1,200 mmol for 7 days. The sheep were housed in metabolism cages and MAP was monitored 24 h/day. Urinary sodium excretion (UNaV) followed changes in sodium intake, with steady-state levels being achieved with similar degrees of rapidity (2-3 days) in nonpregnant and pregnant sheep. At 10 mmol/day sodium intake, MAP was lower (79 +/- 1 vs. 82 +/- 2 mmHg; P < 0.01) and water intake (2,275 +/- 494 vs. 3,286 +/- 725 ml/day; P < 0.001) and 24-h urine volume (1,454 +/- 279 vs. 2,299 +/- 496 ml/day; P < 0.01) were greater in pregnant sheep. All of these variables exhibited direct relationships with increases in sodium intake. Plasma angiotensin II (pANG II) was increased in pregnancy (10.6 +/- 1.6 vs. 24.5 +/- 6.3 pg/ml; P < 0.001) at 10 mmol/day. Elevation of sodium intake suppressed pANG II to minimal levels in nonpregnant sheep, but to only 25% of the control level in pregnant sheep. During pregnancy, the renal function curve representing the steady-state MAP-UNaV relationship was shifted to lower MAP setpoint, but the sodium sensitivity of MAP was unchanged. Also, the inverse relationship of sodium intake and pANG II was blunted, suggesting a reduced role for ANG II in the maintenance of renal function during pregnancy.

Effects of the Fab fragment of digoxin antibody on the natriuresis and increase in blood pressure induced by intracerebroventricular infusion of hypertonic saline solution in rats

1992 ◽  
Vol 82 (6) ◽  
pp. 625-630 ◽  
Author(s):  
Kaoru YAMADA ◽  
Atsuo GOTO ◽  
Chen HUI ◽  
Noriko YAGI ◽  
Tsuneaki SUGIMOTO
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Sodium Excretion ◽  
Urine Volume ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Minor Role ◽  
Fab Fragment ◽  
High Sodium ◽  
Intracerebroventricular Infusion

1. The effects of intravenous injection of Fab fragments of anti-digoxin IgG (Digibind) on the changes in blood pressure, urine volume and urinary sodium excretion after intracerebroventricular infusion of artificial cerebrospinal fluid with normal or high sodium concentration were examined in anaesthetized rats. 2. The biological efficacy of Digibind was confirmed by experiments in vitro and in vivo, which showed that pre-treatment with Digibind completely abolished or significantly attenuated the aortic contractile response or pressor response to digoxin in guinea-pigs. 3. Infusion of high-sodium cerebrospinal fluid, but not normal-sodium cerebrospinal fluid, into the lateral brain ventricle of rats caused marked increases in blood pressure, urine volume and urinary sodium excretion. 4. Digibind did not significantly affect the increases in blood pressure, urine volume and urinary sodium excretion caused by intracerebroventricular infusion of high-sodium cerebrospinal fluid. 5. Digoxin-like immunoreactive factor may play a minor role, if any, in central nervous system-induced natriuresis in rats.

Effects of within-person variability in spot urinary sodium measurements on the associations with blood pressure and risk of cardiovascular disease in 0.5 Million adults in UK Biobank

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Carter ◽  
F Re ◽  
I Hammami ◽  
T Littlejohns ◽  
M Arnold ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Sodium Excretion ◽  
Cox Regression ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
World Health ◽  
Funding Source ◽  
Uk Biobank

Abstract Background Randomised control trials have demonstrated direct positive and causal associations of 24-hr measurements of urinary sodium excretion on blood pressure. However, prospective studies, which often used spot (not 24-hr) measurements of urinary sodium, have reported J-shaped associations with higher risks of cardiovascular disease (CVD) at sodium intake &lt;4 g/day. The reasons for the discrepant results are not fully understood, but have prompted some to question the World Health Organisation's recommendations to restrict sodium intake to &lt;2.3g/day. Purpose We examined the effects of within-person variability in spot urinary sodium (UNa) measurements on immediate and delayed associations of UNa with blood pressure at baseline and at resurvey, and with incident cardiovascular disease in the UK Biobank (UKB). Methods Baseline spot urine samples were measured in 502,619 adults at baseline and in 20,346 participants who were resurveyed at 4 years after baseline. Linear regression was used to assess associations of baseline UNa measurements with systolic blood pressure (SBP; mmHg) at baseline and at resurvey. Cox regression was used estimate the associations between baseline measures of UNa with incident CVD events (recorded from linkage with hospital records). All analyses were adjusted for confounders and corrected for regression dilution bias. Results After excluding participants with prevalent diseases, the primary analyses involved 386,060 adults who were followed-up for a median of 7.8 years, during which ∼13,000 CVD events occurred. Estimated mean (SD) urinary sodium excretion was 77.4 mmol/L (SD 44.4, IQR = 42.8–103.7 mmol/L), and mean SBP/DBP were 137.5/82.3 (SD 18.5/10.1) mmHg, respectively. Within-person variability in UNa was high, with a self-correlation of 0.35 at 4 years between measurements. After adjustment for confounders and correction for regression dilution bias, a 100 mmol/L higher UNa was associated with an immediate 3.2 mmHg higher SBP (95% confidence interval [CI]: 2.8–3.6) in cross-sectional analyses (Figure 1). However, the corresponding associations of baseline UNa with SBP at resurvey was completely attenuated (p=0.20). The predicted risk of CVD was 1.06 (95% CI 1.06–1.07, p&lt;0.001) for a 3.2 mmHg higher SBP, but the observed risk for a 100 mmol/L higher UNa was 0.95 (95% CI 0.82–1.10, p=0.47) (Figure 1). Conclusions While spot measurements of UNa were strongly associated with immediate effects on SBP, the magnitude of within-person variability in UNa precluded detection of associations with SBP several years after baseline or with risk of CVD. The extreme within-person variability in spot UNa may explain the discrepant results of the trials and observational studies of sodium and blood pressure. Figure 1. Spot UNa with SBP and CVD in UK Biobank Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Core funding from the Medical Research Council-Population Health Research Unit, British Heart Foundation

scholarly journals Renal Urotensin II System Plays Roles in the Regulation of Blood Pressure in Dahl Salt-Resistant Rat

2016 ◽  
Vol 2016 ◽  
pp. 1-11
Author(s):  
Fei Wu ◽  
Guanjong Chen ◽  
Aihua Zhang ◽  
Yang Yu ◽  
Minhua Fan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Animal Models ◽  
Receptor Gene ◽  
Urinary Sodium Excretion ◽  
High Salt ◽  
Sodium Absorption ◽  
Urotensin Ii ◽  
High Salt Diet ◽  
Salt Diet ◽  
Regulation Of Blood Pressure

Introduction. Dahl salt-resistant (SR) animal models are similar to peritoneal dialysis patients with fluid volumes overload with normal blood pressure in hemodynamic profiles. We will verify the roles of UII in the regulation of blood pressure in these animal models.Methodology. The Dahl salt-sensitive (SS) and SR rats and UII receptor gene knocked out (KO) mice were placed on a high-salt diet. Renal tissues were performed for the expression of UII in Dahl groups.Results. After high-salt diet for 6 weeks, the systolic blood pressure (SBP) in SR group was significantly lower, accompanied with higher urinary UII levels, higher 24-hour urinary sodium excretion, and higher urinary creatinine clearance in the SR rats in comparison to SS group. The expressions of UII and UT were both upregulated in the kidney tissues of SR group in comparison to SS group (P<0.05). After high-salt diet for 8 weeks, the SBP of the KO group is significantly higher than that of the wild type group.Conclusion. We first demonstrate that renal UII system can play important roles in the regulation of blood pressure in Dahl SR rats which can be highly correlated to its effect on renal tubular sodium absorption.

Abstract 54: Genome-Wide Association Analysis of Gene-Sodium Interactions on Blood Pressure Phenotypes: The GenSalt Study

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Changwei Li ◽  
Jiang He ◽  
James Hixson ◽  
Dongfeng Gu ◽  
Dabeeru Rao ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Meta Analysis ◽  
Snp Array ◽  
Urinary Sodium Excretion ◽  
Dietary Sodium ◽  
Nucleotide Polymorphisms ◽  
Genome Wide ◽  
Inverse Variance ◽  
Meta Analyses

Background: Elevated blood pressure (BP) is a major public health challenge. Although the heritability of BP has been long established, current findings can explain only a small proportion of the BP variability attributed to genetic factors. Recent studies indicate that gene-environmental interactions may help to identify novel BP loci. Hence, the current study aimed to identify genetic variants influencing BP regulation by conducting genome-wide gene-sodium interaction analyses among 1,906 participants of the Genetic Epidemiology Network of Salt-Sensitivity (GenSalt) study. Methods: GenSalt recruited 1,906 Chinese participants from 633 families. At baseline, one 24-hour and two 8-hour urine specimens were collected to measure urinary sodium excretion. Nine BP measurements were taken using a random zero sphygmomanometer. A total of 868,158 autosomal single nucleotide polymorphisms (SNPs) were genotyped using Affymetrix Genomewide Human SNP array 6.0 (Affymetrix, Inc, Santa Clara, CA). Mixed effects models were used to test genome-wide SNP-sodium interactions on BP, adjusting for age, gender, and body mass index. Promising findings (interaction term P <1.00х10 -6 ) from GenSalt were further evaluated for replication among Chinese participants of the Multi-Ethnic Study of Atherosclerosis (MESA) with available data from the database of genotypes and phenotypes (dbGaP). SNP effects in GenSalt and MESA were meta-analyzed using inverse-variance weighted fixed effect models. Results: The meta-analyses identified 3 novel loci that significantly interacted with sodium to influence BP phenotypes. SNP-sodium interactions on systolic BP were identified for NEK2 variant rs10494938 at 1q32.3 (GenSalt P =2.19х10 -6 , MESA P =4.35х10 -4 , and Meta-analysis P = 3.93х10 -8 ). In addition, CASP4 variant rs1944900 at 11q22.3 interacted with sodium to influence both systolic BP (GenSalt P =1.24х10 -9 , MESA P =4.22х10 -2 , and Meta-analysis P = 1.14х10 -10 ) and mean arterial pressure (GenSalt P =1.68х10 -9 , MESA P =4.27х10 -2 , and Meta-analysis P = 1.91х10 -10 ). Furthermore, C9orf3 variant rs17679141 at 9q22.32 interacted with sodium to influence diastolic BP (GenSalt P =2.85х10 -8 , MESA P =4.55х10 -2 , and Meta-analysis P =4.61х10 -9 ). The 3 variants all physically mapped to the intronic regions of their corresponding genes. Conclusion: The current study identified 3 novel loci which may interact with dietary sodium intake to influence BP phenotypes.

scholarly journals Urinary Sodium Excretion and Blood Pressure Relationship across Methods of Evaluating the Completeness of 24-h Urine Collections

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2772
Author(s):  
Abu Mohd Naser ◽  
Feng J. He ◽  
Mahbubur Rahman ◽  
K. M. Venkat Narayan ◽  
Norm R. C. Campbell
Keyword(s):  
Blood Pressure ◽  
Positive Relationship ◽  
Linear Models ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Urine Sodium ◽  
Urine Creatinine ◽  
The Difference ◽  
Multilevel Linear Models

We compared the sodium intake and systolic blood pressure (SBP) relationship from complete 24-h urine samples determined by several methods: self-reported no-missed urine, creatinine index ≥0.7, measured 24-h urine creatinine (mCER) within 25% and 15% of Kawasaki predicted urine creatinine, and sex-specific mCER ranges (mCER 15–25 mg/kg/24-h for men; 10–20 mg/kg/24-h for women). We pooled 10,031 BP and 24-h urine sodium data from 2143 participants. We implemented multilevel linear models to illustrate the shape of the sodium–BP relationship using the restricted cubic spline (RCS) plots, and to assess the difference in mean SBP for a 100 mmol increase in 24-h urine sodium. The RCS plot illustrated an initial steep positive sodium–SBP relationship for all methods, followed by a less steep positive relationship for self-reported no-missed urine, creatinine index ≥0.7, and sex-specific mCER ranges; and a plateaued relationship for the two Kawasaki methods. Each 100 mmol/24-h increase in urinary sodium was associated with 0.64 (95% CI: 0.34, 0.94) mmHg higher SBP for self-reported no-missed urine, 0.68 (95% CI: 0.27, 1.08) mmHg higher SBP for creatinine index ≥0.7, 0.87 (95% CI: 0.07, 1.67) mmHg higher SBP for mCER within 25% Kawasaki predicted urine creatinine, 0.98 (95% CI: −0.07, 2.02) mmHg change in SBP for mCER within 15% Kawasaki predicted urine creatinine, and 1.96 (95% CI: 0.93, 2.99) mmHg higher SBP for sex-specific mCER ranges. Studies examining 24-h urine sodium in relation to health outcomes will have different results based on how urine collections are deemed as complete.

Hydration Status and Sodium Balance of Endurance Runners Consuming Postexercise Supplements of Varying Nutrient Content

2015 ◽  
Vol 25 (5) ◽  
pp. 471-479 ◽  
Author(s):  
J. Luke Pryor ◽  
Evan C. Johnson ◽  
Jeffery Del Favero ◽  
Andrew Monteleone ◽  
Lawrence E. Armstrong ◽  
...  
Keyword(s):  
Body Mass ◽  
Sodium Intake ◽  
Urine Volume ◽  
Nutrient Content ◽  
Urinary Sodium Excretion ◽  
Nutritional Supplement ◽  
Running Economy ◽  
Urine Specific Gravity ◽  
Sodium Balance ◽  
Hydration Status

Postexercise protein and sodium supplementation may aid recovery and rehydration. Preserved beef provides protein and contains high quantities of sodium that may alter performance related variables in runners. The purpose of this study was to determine the effects of consuming a commercial beef product postexercise on sodium and water balance. A secondary objective was to characterize effects of the supplementation protocols on hydration, blood pressure, body mass, and running economy. Eight trained males (age = 22 ± 3 y, V̇O2max = 66.4 ± 4.2 ml·kg-1·min-1) completed three identical weeks of run training (6 run·wk-1, 45 ± 6 min·run-1, 74 ± 5% HRR). After exercise, subjects consumed either, a beef nutritional supplement (beef jerky; [B]), a standard recovery drink (SRD), or SRD+B in a randomized counterbalanced design. Hydration status was assessed via urinary biomarkers and body mass. No main effects of treatment were observed for 24 hr urine volume (SRD, 1.7 ± 0.5; B, 1.8 ± 0.6; SRD+B, 1.4 ± 0.4 L·d-1), urine specific gravity (1.016 ± 0.005, 1.018 ± 0.006, 1.017 ± 0.006) or body mass (68.4 ± 8.2, 68.3 ± 7.7, 68.2 ± 8.1 kg). No main effect of treatment existed for sodium intake—loss (-713 ± 1486; -973 ± 1123; -980 ± 1220 mg·d-1). Mean arterial pressure (81.0 ± 4.6, 81.1 ± 7.3, 83.8 ± 5.4 mm Hg) and average exercise running economy (V̇O2: SRD, 47.9 ± 3.2; B, 47.2 ± 2.6; SRD+B, 46.2 ± 3.4 ml·kg-1·min-1) was not affected. Urinary sodium excretion accounted for the daily sodium intake due to the beef nutritional supplement. Findings suggest the commercial beef snack is a viable recovery supplement following endurance exercise without concern for hydration status, performance decrements, or cardiovascular consequences.

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