High Dietary Sodium Intake Research Articles

Blockade of the renin–angiotensin system and renal tissue oxygenation as measured with BOLD-MRI in patients with type 2 diabetes

AimTo assess whether blockade of the renin–angiotensin system (RAS), a recognized strategy to prevent the progression of diabetic nephropathy, affects renal tissue oxygenation in type 2 diabetes mellitus (T2DM) patients. MethodsProspective randomized 2-way cross over study; T2DM patients with (micro)albuminuria and/or hypertension underwent blood oxygenation level-dependent magnetic resonance imaging (BOLD-MRI) at baseline, after one month of enalapril (20mgqd), and after one month of candesartan (16mgqd). Each BOLD-MRI was performed before and after the administration of furosemide. The mean R2* (=1/T2*) values in the medulla and cortex were calculated, a low R2* indicating high tissue oxygenation. ResultsTwelve patients (mean age: 60±11 years, eGFR: 62±22ml/min/1.73m2) completed the study. Neither chronic enalapril nor candesartan intake modified renal cortical or medullary R2* levels. Furosemide significantly decreased cortical and medullary R2* levels suggesting a transient increase in renal oxygenation. Medullary R2* levels correlated positively with urinary sodium excretion and systemic blood pressure, suggesting lower renal oxygenation at higher dietary sodium intake and blood pressure; cortical R2* levels correlated positively with glycemia and HbA1c. ConclusionRAS blockade does not seem to increase renal tissue oxygenation in T2DM hypertensive patients. The response to furosemide and the association with 24h urinary sodium excretion emphasize the crucial role of renal sodium handling as one of the main determinants of renal tissue oxygenation.

Characteristics of hypertension in Chinese and their relevance for the choice of antihypertensive drugs

According to the 4th National Nutrition and Health Survey in 2002, the prevalence of hypertension in China was 18.8%. Despite that, the treatment rate among hypertensive patients was 82%, the control rate remained low in persons with hypertension (6%), because of the low awareness in general (30%) and the low control rate among treated hypertensive patients (25%). One of the major reasons for the increasing prevalence of hypertension is unbalance of dietary sodium and potassium intakes. In the International Study of Macro/Micro-nutrients and Blood Pressure (INTERMAP), Chinese, compared with American, British, and Japanese populations, had highest dietary sodium intakes and lowest potassium intakes, leading to a two to three times higher sodium/potassium ratio. High dietary sodium intakes may change the circadian rhythm of 24 h blood pressure, which is characterized by a higher night-time blood pressure. Indeed, the prevalence of isolated night-time hypertension, defined as a night-time blood pressure of at least 120 mmHg systolic or 70 mmHg diastolic and a daytime systolic/diastolic blood pressure less than 135/85 mmHg, was higher in Chinese than in Europeans. The complications of hypertension are also different across ethnicities, being mainly stroke instead of myocardial infarction in Chinese. Blood pressure lowering provides more protection against stroke than myocardial infarction, and calcium channel blockers provide more protection against stroke than other classes of antihypertensive drugs. Current Chinese hypertension guidelines recommend calcium channel blockers as the first of the five classes of antihypertensive drugs for stage 1 and low-risk hypertension.

Abstract 425: High Sodium Excretion is not Associated with Reduced Vasodilation in Healthy African American Adults

Background: High dietary sodium (Na) intake has been shown to be related to the development of endothelial dysfunction and hypertension. Urinary sodium excretion in people with normal renal function can indirectly reflect the level of dietary sodium intake. The purpose of the study was to test whether high urine Na excretion was independent from other risk factors and related to the compromised endothelial-dependent (fiow-mediated dilation [FMD]) and/or endothelium-independent (nitroglycerin-induced dilation [NMD]) in normotensive African Americans. Normotensives were studied in order to eliminate the influence of hypertension. METHODS: Urine was collected for 24 hr in 30 subjects aged 41-63 yrs with normal blood pressure (125.7 ± 9.7/81 ± 7.1 mmHg). 16 subjects had Na excretion <150 mmol (99.6 ± 24.8 mmol) and were classified as the Normal Na excretion group and 14 subjects had Na excretion ≥150 mmol/g (186.5 ± 27.1 mmol) and were classified as the High Na excretion group. FMD was measured after 5-min cuff occlusion and NMD was measured after application of 0.8 mg nitroglycerin using Doppler ultrasound. The maximum FMD- and NMD-diameters and FMD/NMD ratio were calculated. Results: There were no differences in other dietary factors, age, body mass index, blood pressure, or physical activity levels between the groups. Plasma concentrations of cholesterol, glucose, antioxidant status and inflammatory markers did not differ between groups. FMD (Normal: 7.4 ± 2.9% vs. High: 9.5 ± 3.6%; p=0.09) and NMD (Normal: 17.9 ± 6.3% vs. High: 27.8 ± 18.1%; p=0.07) and true peak FMD/NMD ratio (Normal: 0.45 ± 0.22 vs. High: 0.38 ± 0.11; p=0.26) were not different between groups. No significant correlations were found between 24hr Na excretion and FMD (r=0.332; p=0.073), NMD (r=0.356; p=0.053) or FMD/NMD ratio(r=0.112; p=0.554) in the entire study group. Conclusion: High Na excretion was not associated with reduced endothelial responsiveness in healthy African Americans with normal blood pressure. These results suggest that high Na intake may not be predictive of endothelial dysfunction in putatively healthy populations.

Moderation of dietary sodium potentiates the renal and cardiovascular protective effects of angiotensin receptor blockers

Dietary sodium restriction has been shown to enhance the short-term response of blood pressure and albuminuria to angiotensin receptor blockers (ARBs). Whether this also enhances the long-term renal and cardiovascular protective effects of ARBs is unknown. Here we conducted a post-hoc analysis of the RENAAL and IDNT trials to test this in patients with type 2 diabetic nephropathy randomized to ARB or non-renin-angiotensin-aldosterone system (non-RAASi)-based antihypertensive therapy. Treatment effects on renal and cardiovascular outcomes were compared in subgroups based on dietary sodium intake during treatment, measured as the 24-h urinary sodium/creatinine ratio of 1177 patients with available 24-h urinary sodium measurements. ARB compared to non-RAASi-based therapy produced the greatest long-term effects on renal and cardiovascular events in the lowest tertile of sodium intake. Compared to non-RAASi, the trend in risk for renal events was significantly reduced by 43%, not changed, or increased by 37% for each tertile of increased sodium intake, respectively. The trend for cardiovascular events was significantly reduced by 37%, increased by 2% and 25%, respectively. Thus, treatment effects of ARB compared with non-RAASi-based therapy on renal and cardiovascular outcomes were greater in patients with type 2 diabetic nephropathy with lower than higher dietary sodium intake. This underscores the avoidance of excessive sodium intake, particularly in type 2 diabetic patients receiving ARB therapy.

Characteristics of Hypertension in the Chinese Population

In China, the prevalence of hypertension is currently 18.8%, and a major risk factor for hypertension is unbalanced dietary sodium and potassium intakes. High dietary sodium intake may change the circadian rhythm of 24-h blood pressure, which is characterized by a higher nighttime blood pressure. The prevalence of isolated nighttime hypertension, defined as a nighttime blood pressure of at least 120mm Hg systolic or 70mmHg diastolic and a daytime systolic/diastolic blood pressure less than 135/85mmHg, is higher in Chinese than in Europeans. The complications of hypertension are also different across ethnicities, being mainly stroke instead of myocardial infarction in Chinese. Lowering of blood pressure provides more protection against stroke than against myocardial infarction, and calcium channel blockers provide more protection against stroke than do other classes of antihypertensive drugs. Current Chinese hypertension guidelines recommend calcium channel blockers as the most suitable class of drugs of the five classes of antihypertensive drugs.

High Sodium Intake Is Associated With Masked Hypertension in Japanese Patients With Type 2 Diabetes and Treated Hypertension

Knowledge regarding the association between dietary sodium intake and the incidence of masked hypertension is limited. A total of 193 Japanese type 2 diabetic outpatients who had been treated with antihypertensive agents and with office blood pressures <140/90 mm Hg were recruited. Masked hypertension was defined as having office blood pressure <140/90 mm Hg and 24-h mean ambulatory blood pressure ≥130/80 mm Hg. The dietary sodium intake was estimated by measuring the 24-h urinary sodium excretion. Masked hypertension was found in 128 (66.3%) patients. An age- and sex-adjusted univariate logistic regression analysis showed that urinary albumin excretion, renin-angiotensin system inhibitor use, office systolic blood pressure, and amount of dietary sodium intake were significantly associated with masked hypertension. A multivariate logistic regression analysis also identified an older age, renin-angiotensin system inhibitor use, an office elevated systolic blood pressure, and high dietary sodium intake to be independently associated with masked hypertension. When compared with those who consumed a low salt diet (sodium <120 mEq/day), the odds ratio for the risk of exhibiting masked hypertension in patients who consumed a medium salt diet (sodium 120 to <200 mEq/day) or a high salt diet (sodium ≥200 mEq/day) were 5.3 (P < 0.001) and 12.6 (P < 0.001), respectively. Masked hypertension is a common feature in type 2 diabetic patients being treated for hypertension. The observed association with sodium intake raised the hypothesis that excessive sodium intake may play a part in the genesis of masked hypertension in these patients.

Dietary sodium and clinical outcome in hemodialysis: where do we stand and what is next?

The association of dietary sodium and outcome is widely studied in the general population, but less is known in hemodialysis patients. The evidence supporting daily dietary sodium intake of 2 g on hemodialysis is not strong. Mc Causland et al. found that higher dietary sodium intake was marginally associated with a higher ultrafiltration requirement and mortality, but not with blood pressure. Well-designed clinical trials are needed to examine the association of dietary sodium modification and outcomes in hemodialysis patients.

Differential effects of dietary sodium intake on blood pressure and atherosclerosis in hypercholesterolemic mice

The amount of dietary sodium intake regulates the renin angiotensin system (RAS) and blood pressure, both of which play critical roles in atherosclerosis. However, there are conflicting findings regarding the effects of dietary sodium intake on atherosclerosis. This study applied a broad range of dietary sodium concentrations to determine the concomitant effects of dietary sodium intake on the RAS, blood pressure, and atherosclerosis in mice. Eight-week-old male low-density lipoprotein receptor −/− mice were fed a saturated fat-enriched diet containing selected sodium concentrations (Na 0.01%, 0.1%, or 2% w/w) for 12 weeks. Mice in these three groups were all hypercholesterolemic, although mice fed Na 0.01% and Na 0.1% had higher plasma cholesterol concentrations than mice fed Na 2%. Mice fed Na 0.01% had greater abundances of renal renin mRNA than those fed Na 0.1% and 2%. Plasma renin concentrations were higher in mice fed Na 0.01% (14.2±1.7 ng/ml/30 min) than those fed Na 0.1% or 2% (6.2±0.6 and 5.8±1.6 ng/ml per 30 min, respectively). However, systolic blood pressure at 12 weeks was higher in mice fed Na 2% (138±3 mm Hg) than those fed Na 0.01% and 0.1% (129±3 and 128±4 mmHg, respectively). In contrast, mice fed Na 0.01% (0.17±0.02 mm2) had larger atherosclerotic lesion areas in aortic roots than those fed Na 2% (0.09±0.01 mm2), whereas lesion areas in mice fed Na 0.1% (0.12±0.02 mm2) were intermediate between and not significantly different from those in Na 0.01% and Na 2% groups. In conclusion, while high dietary sodium intake led to higher systolic blood pressure, low dietary sodium intake augmented atherosclerosis in hypercholesterolemic mice.

Dietary sodium intake deleteriously affects blood pressure in a normotensive population

Western dietary pattern, and particularly high dietary sodium intake (DSI), is recognized for its detrimental impact on blood pressure (BP). This paper examined the association of DSI with BP in Nunavik Inuit (Québec), a population known to have an optimal BP on average. In a population-based study, we recruited 421 normotensive participants aged 18-74 years from 14 coastal villages, situated north of the 55th parallel. BP, biochemistry and anthropometry were obtained. DSI was assessed by a 24-h dietary recall. Mean (s.e.) DSI was higher in men than in women (2358 (101) vs. 1702 (100) mg/d, P<0.0001). Similar gender difference was found in systolic BP (118 (0.7) vs. 111 (0.6) mm Hg; P<0.0001). After adjustment for confounders, we found a positive association between BP and DSI (all P<0.05). In a normotensive population, BP shows a linear relationship with DSI. Our results emphasize the potent deleterious impact of DSI on BP.

The role of α1B-ARs in regulating renal hemodynamic and renal functions in hypertensive rats; impact of high dietary sodium intake

Background: Renal α1B-adrenoreceptors (α1-ARs) contributes to the pathogenesis of hypertension in spontaneously hypertensive rats (SHR). The present study examined the role of α1B-ARs in renal hemodynamic and tubular functions in SHR subjected to high-salt diet (SHRHNa) for 6 weeks. Methods: Renal cortical vasoconstriction to noradrenaline (NA), phenylephrine (PE), and methoxamine (ME) in presence and absence of chloroethylclonidine (CEC) was measured in SHRHNa and SHR on normal sodium diet (SHRNNa). Renal tubular functional responses to PE and CEC were assessed as a measure of insulin clearance. Results: SHRHNa showed no significant change in the mean arterial pressure (MAP) as compared to SHRNNa. SHRHNa expressed enhanced renal cortical vascular sensitivity to NA, PE, and ME. Furthermore, renal vasoconstrictor response to NA, PE and ME was accentuated in the presence of CEC in SHRNNa. On the other hand in SHRHNa, renal cortical vasoconstriction to NA and ME was inhibited by CEC. However tubular response to PE was inhibited by CEC in SHRNNa and remains unaffected in SHRHNa. Conclusion: Thus it is concluded that, augmented α1-adrenergic response to adrenergic stimuli contribute to salt-related increase in renal vascular sensitivity in SHRHNa and these changes were independent of any further increase in MAP in SHRHNa. Irrespective of dietary sodium changes, α1-ARs are involved in mediation of tubular functions like antinatriuresis and antidiuresis of SHR. In addition, α1B-ARs are the functional subtypes that mediate renal cortical vasoconstriction in SHRHNa and tubular function in SHRNNa, while high sodium in SHR did not influence the functionality of α1B-ARs in mediating tubular functions.

Sex differences in salt sensitivity to nitric oxide dependent vasodilation in healthy young adults

Dietary sodium and blood pressure regulation differs between normotensive men and women, an effect which may involve endothelial production of nitric oxide (NO). Therefore, we tested the hypothesis that differences in the NO component of endothelium-dependent vasodilation between low and high dietary sodium intake depend on sex. For 5 days prior to study, healthy adults consumed a controlled low-sodium diet (10 mmol/day, n = 30, mean age ± SE: 30 ± 1 yr, 16 men) or high-sodium diet (400 mmol/day, n = 36, age 23 ± 1 yr, 13 men). Forearm blood flow (FBF, plethysmography) responses to brachial artery administration of acetylcholine (ACh, 4 μg·100 ml tissue(-1)·min(-1)) were measured before and after endothelial NO synthase inhibition with N(G)-monomethyl-l-arginine (l-NMMA, 50 mg bolus + 1 mg/min infusion). The NO component of endothelium-dependent dilation was calculated as the response to ACh before and after l-NMMA accounting for changes in baseline FBF: [(FBF ACh - FBF baseline) - (FBF ACh(L-NMMA) - FBF baseline(L-NMMA))]. This value was 5.7 ± 1.3 and 2.5 ± 0.8 ml·100 ml forearm tissue(-1)·min(-1) for the low- and high-sodium diets, respectively (main effect of sodium, P = 0.019). The sodium effect was larger for the men, with values of 7.9 ± 2.0 and 2.2 ± 1.4 for men vs. 3.1 ± 1.3 and 2.7 ± 1.0 ml·100 ml forearm tissue(-1)·min(-1) for the women (P = 0.034, sex-by-sodium interaction). We conclude that the NO component of endothelium-dependent vasodilation is altered by dietary sodium intake based on sex, suggesting that endothelial NO production is sensitive to dietary sodium in healthy young men but not women.

Unraveling the Mechanism of Renin-Angiotensin- Aldosterone System Activation and Target Organ Damage in Hypertensive Blacks

See related article, pp 62–69 The International Society on Hypertension in Blacks consensus statement in 2010 noted that, in the setting of high dietary sodium intake, hypertensive blacks have particularly impressive responses to renin-angiotensin-aldosterone system (RAAS) blockade.1 The statement went on to point out that the excessive target-organ damage (TOD) in hypertensive blacks can be attributed to RAAS activation. Although a normal-to-“high-renin” hypertensive state is most prevalent, the classic hypertension literature has categorized blacks as typically having a “low-renin” state.2 There is somewhat of a paradox in the observation that blacks, despite having a low-renin state, have high serum aldosterone concentrations.3 Blacks experience disproportionately higher rates of hypertension-related TOD compared with whites.4 The mediators of the higher rates of TOD noted in blacks are most likely directly attributed to high levels of downstream mediators of the RAAS, such as aldosterone and angiotensin II. The mechanism by which a low-renin state can be associated with such an apparently active RAAS is not clearly defined. The article by Michel et al,5 in this issue of Hypertension , addresses the mechanism by which RAAS activation affects blood pressure (BP) …

J-036 THE PREVALENCE OF HYPERTENSIVE PATIENTS WITH HIGH SODIUM CONSUMPTION IN HYPERTENSION CLINIC AT SIRIRAJ HOSPITAL

Background High dietary sodium intake is associated with the development of hypertension which is one of the most important risk factors for cardiovascular disease (CVD), stroke and renal failure. Decreasing sodium intake will contribute to risk reduction in developing the diseases. The level of salt intake in our hypertensive patients can be monitored outpatiently and epidemiologic characteristics among those high salt intake can be sorted out to improve hypertension management. Methods A cross-sectional study which enrolled 320 hypertensive patients in hypertension clinic at Siriraj Hospital was carried out from September 2010 to January 2011. Epidemiologic data e.g. age, sex, body mass index (BMI), duration of treatment, education, salary, frequency of salty food consumed/week and clinical data e.g. creatinine clearance and anti-hypertensive drug(s) received were collected using pre-defined questionnaires. 24-hour urine for 2 days to determine average amount of urine sodium/day were collected by volunteers. Urine sodium of >100 mmol/day were considered high salt intake. Correlations of those with high salt intake with all variables were done. Results The prevalence of high salt intake was 73.4%. The mean amount of daily sodium intake was 148 mmol/day (3,404 mg/day). Rate of high salt intake was found in males more than females (p = 0.001), those of <60 year old (p = 0.012), those with higher education (p < 0.001), higher salary (p < 0.001) and those who have self-own business (p = 0.01). About three-quarters (76.3%) of those patients who knew the effect of salt on blood pressure consumed high salt diet. Conclusions This study revealed that nearly three-quarters of hypertensive patients attended at hypertension clinic still consumed high salt diet. Those patients with certain epidemilogic characteristics were found to consume high sodium diet. Simple verbal instructions for patients to consume low salt diet seem to be insufficient in clinical practice.

High Dietary Sodium Intake among Young Children in Vancouver, British Columbia

Objective: To determine the intake distribution and food sources of sodium among young children.Methods: Dietary intake was determined for 190 children, 16 months to 6 years of age, using a food frequency questionnaire completed by interviewing a parent. Dietary intake of all nutrients, including dietary sodium, was analyzed. The major food sources of sodium were assessed by grouping foods into categories based on Canada's Food Guide, with subsequent subdivision into food type categories.Results: Dietary sodium intakes were skewed, with a median intake of 2021 mg/d and 5th–95th percentile range of 888–3975 mg/d. The sodium intake of 91.6% of children was above the recommended 1000 or 1200 mg/d for children 1–3 or 3–6 years, respectively, and 85% and 54% had intakes above the tolerable upper limits of 1500 and 1900 mg/d, respectively. The 5 food sources providing the highest amount of sodium were soups, processed/fast foods, dairy products, breads, and processed meats.Conclusion: Children are vulnerable to high sodium intake as a result of their food patterns and the high sodium content of these foods. This report demonstrates that Canadian children have high sodium intakes. Knowledge of feeding practices involving high-sodium foods can assist parents and caregivers in reducing the high sodium intake of young children.

Impact of elevated dietary sodium intake on NAD(P)H oxidase and SOD in the cortex and medulla of the rat kidney

Pathophysiological states, including cardiovascular and renal diseases, are characterized by oxidative stress but what is less clear is whether physiological challenges incur a degree of altered oxidative metabolism. To this end, this study examined whether exposure to a high dietary sodium intake could cause an oxidative stress at the kidney. Animals, placed on either 0.3% or 3% sodium diets for 2 wk, were given a lethal dose of anesthetic, and kidneys were removed to analyze both NAD(P)H oxidase (NOX) and superoxide dismutase (SOD) expression and activities in the cortex and medulla. Placing animals on the high-sodium diet raised sodium and water excretion and caused an approximately 14-fold increase in urinary excretion of 8-isoprostane, a marker of oxidative stress, which was attenuated by chronic treatment with apocynin to prevent NAD(P)H oxidase activity. The protein expression of the NAD(P)H oxidase subunits NOX2 and p47(phox) and overall NAD(P)H oxidase activity were approximately doubled in the cortex of the rats on the high-sodium diet compared with those on the normal sodium intake while both SOD activity and expression were unchanged. By contrast, neither NOX nor SOD protein expression or activity were altered in the medulla when the rats were placed on the high-sodium intake. These data suggest that an elevation in dietary sodium intake can lead to increased generation of reactive oxygen species and a state of oxidative stress in the cortex but not to such a degree that it extends to the medulla.

Dietary sodium and the renal responses to Angiotensin1–7 (ANG1–7)

This study investigated how the renal excretory actions of ANG1–7 were altered when the renin‐angiotensin system (RAS) was activated or suppressed following a period of low or high dietary sodium intake. Male Wistar rats were fed a low (0.03%), normal (0.3%) or a high (3.0%) sodium diet for 2 weeks. The animals were anaesthetised with chloralose/urethane and prepared for the measurement of blood pressure (BP), iv infusion of saline (0.9%NaCl, 3.0 ml/h). Cannulae were placed in the left ureter for urine collection and at the cortico‐medullary border for saline or ANG1–7 infusion at 1.0ml/h. Four 20 min clearances were taken, two before and two 45min after either saline or ANG1–7 (9×10−7M) infusion. Data, means ±SEM were analysed using Student's t test. Infusion of saline had no effect on BP or any renal functional parameter. ANG1–7 infusion in rats on the normal diet did not change BP, at 99±4mmHg, but urine flow, at 18.1±1.3μl/min/kg, and fractional sodium excretion (FENa), at 0.6±0.1, were increased by 24 and 25% (both P&lt;0.05). In the low salt rats, ANG1–7 caused a greater response in FENa, of some 2–3 fold (P&lt;0.05) whereas in the high salt rats, it was blunted, being only 60% of the response in normal rats. These findings demonstrate a dependency of the excretory responses to ANG1–7 on the endogenous levels of RAS.

Benefits of dietary sodium restriction in the management of chronic kidney disease

To evaluate the role of restricting dietary sodium intake in chronic kidney disease (CKD) and its complications. A consistent line of evidence shows that high dietary sodium intake is a determinant of therapy resistance to blockade of the renin-angiotensin-aldosterone system (RAAS). Addition of sodium restriction to RAAS blockade or to RAAS blockade combined with a diuretic permits a further reduction in urinary protein excretion of approximately 30%, which could be expected to reduce long-term renal risk by 25%. High sodium intake increases blood pressure and proteinuria, induces glomerular hyperfiltration and blunts the response to RAAS blockade. Although recommended in international guidelines, sodium restriction is not a spearhead in treating renal patients. Sodium status is only rarely mentioned in recent large intervention studies in CKD. Sodium intake in CKD is similar to that in the general population. Reduction of sodium intake to the target of 50-85 mmol/24 h in patients with CKD reduces blood pressure and proteinuria, the latter by approximately 30%, and should be actively pursued to improve outcome in CKD.

Influence of high dietary sodium intake on the functional subtypes of α1‐adrenoceptors in the renal cortical vasculature of Wistar–Kyoto rats

1 Increased renal vascular resistance is one renal functional abnormality that contributes to hypertension, and alpha(1)-adrenoceptors play a pivotal role in modulating this renal vascular resistance. This study investigates the functional contribution of alpha(1)-adrenoceptor subtypes in the renal cortical vasculature of Wistar-Kyoto rats on a normal sodium diet (WKYNNa) compared with those given saline to drink for 6 weeks (WKYHNa). 2 The renal cortical vascular responses to the adrenergic agonists noradrenaline (NA), methoxamine (ME) and phenylephrine (PE) were measured in WKYHNa and WKYNNa rats either in the absence (the control phase) or presence of chloroethylclonidine (CEC), an alpha(1B)-adrenoceptor antagonist, 5-methylurapidil (5-MeU), an alpha(1A) antagonist, or BMY7378, an alpha(1D) antagonist. 3 Results showed a greater renal cortical vascular sensitivity to NA, PE and ME in the WKYHNa compared with WKYNNa rats (P < 0.05). Moreover, 5-MeU and BMY7378 attenuated adrenergically induced renal cortical vasoconstriction in WKYHNa and WKYNNa rats; this response was largely blunted in CEC-treated WKYHNa rats (all P < 0.05) but not in CEC-treated WKYNNa rats. 4 The data suggest that irrespective of dietary sodium content, in Wistar-Kyoto rats alpha(1A)- and alpha(1D)-subtypes are the major alpha(1)-adrenoceptors in renal cortical vasculature; however, there appears to be a functional involvement of alpha(1B)-adrenoceptors in the WKYHNa rats.

Sweat Sodium Concentration in NFL Players during Dietary Sodium Supplementation compared to when they are not Supplemented

High dietary sodium (Na+) intake, compared to low or moderate intake, should cause athletes to secrete sweat high in Na+ concentration [SwtNa+]. We have Na+ supplemented NFL players for several years but have not investigated the effect of supplementation on [SwtNa+]. PURPOSE: To compare [SwtNa+], total Na+ losses, fluid intake and weight loss in NFL players during a practice the first week of training camp while Na+ supplemented (Na+Suppl) compared to those same measures a week later when they were unsupplemented (UnSuppl). METHODS: Data were collected on days 5 - 7 while players were supplemented and then days 10 - 12 when players were un-supplemented for a minimum of 3 days. Na+Suppl consisted of each player receiving table salt dissolved in juice in an amount equal to 50% of their individual daily Na+ losses calculated from previous data. Twelve players volunteered, 3 were injured and did not practice the 1st week and 2 asked to be put back on the supplementation, therefore, 7 NFL players with age = 26.6 ± 2 y, height = 186.4 ± 8 cm, mass =110 ± 24 kg, BSA = 2.33 ± 0.25m2 participated. After the skin of the right upper forearm of each subject was prepped with alcohol and de-ionized water, a sterile sweat patch was applied and secured with impermeable tape. The patches where removed during practice, placed in sterile, siliconized tubes and centrifuged on site. The neat sweat samples were frozen and later assayed using flame photometry. Sweat loss was calculated by change in mass adjusted for fluids consumed and urine produced during practice. Comparisons were made using paired t-tests. RESULTS: WBGT assessed 3 times during practices were not different between days 5-7 and days 10-12 nor were and length of practices. Subjects consumed more fluid during practice while NaSupp (2.13 ± 1.2 L) versus (1.34 ± .75 L), p = .02. There were no differences in [SwtNa+] (NaSuppl = 52.4 ± 28 mmol·l-1 and UnSuppl = 55 ± 26 mmol·l-1 ranging from 14.3 to 91 mmol·l-1), total sodium losses (NaSuppl = 3023 ± 1987 mg and UnSuppl = 2642 ± 1304mg), SwtR (NaSuppl =1.23 ± 0.47 and UnSuppl = 1.22 ± 0.4 l·hr-1), sweat loss (NaSuppl = 2.8 ±1.4 and UnSuppl = 2.23 ± .81 L, urine volume or weight loss. CONCLUSIONS: Dietary Na+ intake equal to 50% of daily sweat Na+ losses in NFL players did not result in higher [SwtNa+] or Na+ losses, but did promote higher fluid consumption during practice.

High dietary sodium intake sensitizes the pressor and renal sympathetic nerve activity responses to peripheral and spinal vasopressin infusion

Vasopressinergic (AVP) activation of spinal and vascular V1 receptors may contribute to the sensitized blood pressure (BP) and renal sympathoexcitatory (RSNA) responses to ANGII and ANGIII ICV infusion after high Na+ (HNa+) intake. This hypothesis was tested by comparing the BP and RSNA responses to intravenous (IV) or intrathecal (IT) AVP infusion in male Wistar rats fed a normal Na+ (NNa+, 0.3%) or HNa+ (3.0%) diet for six weeks. At 11 weeks of age, rats were anaesthetized (1ml IP chloralose/urethane) and instrumented with arterial and IV cannulae. The tip of the IT cannula was placed at spinal vertebra T13. RSNA was recorded from the left kidney. ΔBP (mmHg) or ΔRSNA (%baseline) were measured after IV AVP (1, 3, 5 or 10ng/0.2ml; NNa+ n=6, HNa+=7) or IT AVP (1, 5, 10, 20μM; 10μL/2min; NNa+ =7, HNa+ = 5), respectively. Data are presented as mean ± SE. P&lt;0.05 indicated significance. Basal BP (mmHg, NNa+ 89±4, HNa+ 95±4) and RSNA (μV/s, NNa+ 15.1±4.6 vs HNa+10.4±3.0) were similar between groups. ΔBP was greater to all doses of IV AVP in HNa+ (P&lt;0.001). ΔRSNA was greater in HNa+ after 1μM (NNa+:1.0±2.0% vs HNa+: 8.2±2.0%, P&lt;0.05) and 5μM (NNa+: 3.2± 1.2% vs HNa+: 10.2±1.9%, P&lt;0.05) IT AVP. These results show that HNa+ intake sensitizes both AVP induced peripheral vasoconstriction and spinal V1 mediated RSNA, which together may contribute to the development of hypertension. Funding: HRB RP/2004/17.