Supplementation Reduces Blood Pressure Research Articles

Defective natriuresis contributes to hyperkalemia in db/db mice during potassium supplementation.

Potassium supplementation reduces blood pressure and the occurrence of cardiovascular diseases, with K + -induced natriuresis playing a potential key role in this process. However, whether these beneficial effects occur in diabetes remains unknown. In this study, we examined the impact of high-K + intake on renal Na + /K + transport by determining the expression of major apical Na + transporters, diuretics responses (as a proxy for specific Na + transporter function), urinary Na + /K + excretion, and plasma Na + /K + concentrations in db/db mice, a model of type 2 diabetes mellitus. Although db/m mice exhibited increased fractional excretion of sodium (FE Na ) and fractional excretion of potassium (FE K ) under high-K + intake, these responses were largely blunted in db/db mice, suggesting impaired K + -induced natriuresis and kaliuresis in diabetes. Consequently, high-K + intake increased plasma K + levels in db/db mice, which could be attributed to the abnormal activity of sodium-hydrogen exchanger 3 (NHE3), sodium-chloride cotransporter (NCC), and epithelial Na + channel (ENaC), as high-K + intake could not effectively decrease NHE3 and NCC and increase ENaC expression and activity in the diabetic group. Inhibition of NCC by hydrochlorothiazide could correct the hyperkalemia in db/db mice fed a high-K + diet, indicating a key role for NCC in K + -loaded diabetic mice. Treatment with metformin enhanced urinary Na + /K + excretion and normalized plasma K + levels in db/db mice with a high-K + diet, at least partially, by suppressing NCC activity. Collectively, the impaired K + -induced natriuresis in diabetic mice under high-K + intake may be primarily attributed to impaired NCC-mediated renal K + excretion, despite the role of NHE3.

L-Citrulline Supplementation Reduces Blood Pressure and Myocardial Infarct Size under Chronic Intermittent Hypoxia, a Major Feature of Sleep Apnea Syndrome.

Intermittent hypoxia (IH) is a landmark of obstructive sleep apnea (OSA) at the core of the cardiovascular consequences of OSA. IH triggers oxidative stress, a major underlying mechanism for elevated blood pressure (BP) and increased infarct size. L-citrulline is an amino acid that has been demonstrated to be protective of the cardiovascular system and exert pleiotropic effects. Therefore, we tested the impact of citrulline supplementation on IH-induced increase in BP and infarct size. Four groups of rats exposed to normoxia (N) or IH [14 days (d), 8 h/day, 30 s-O2 21%/30 s-O2 5%] and were supplemented or not with citrulline (1 g·kg-1·d-1). After 14 d, BP was measured, and hearts were submitted to global ischemia-reperfusion to measure infarct size. Histological and biochemical analyses were conducted on hearts and aorta to assess oxidative stress. Citrulline significantly reduced BP (-9.92%) and infarct size (-18.22%) under IH only. In the aorta, citrulline supplementation significantly decreased superoxide anion and nitrotyrosine levels under IH and abolished the IH-induced decrease in nitrite. Citrulline supplementation significantly decreased myocardial superoxide anion levels and xanthine oxidase enzyme activity under IH. Citrulline shows a cardioprotective capacity by limiting IH-induced pro-oxidant activity. Our results suggest that citrulline might represent a new pharmacological strategy in OSA patients with high cardiovascular risk.

MO389: Klotho Supplementation Reverses Renal Dysfunction and Interstitial Fibrosis in Remnant Kidney

Abstract BACKGROUND AND AIMS Several studies demonstrate that klotho shows renoprotective actions. However, it has not been assessed whether klotho supplementation is able to reverse the renal injury. METHOD In the present study, the effects of klotho protein supplementation on remnant rat kidneys were assessed using three groups: renal ablation for 4 weeks, renal ablation for 12 weeks and klotho supplementation (20 μg/kg/day). RESULTS Klotho supplementation suppressed blood pressure, albuminuria, renal renin-angiotensin system (RAS), serum phosphate and fibroblast growth factor (FGF) 23 levels, fibrosis index, renal expression of transforming growth factor β and collagen I. Klotho protein supplementation increased glomerular filtration rate (GFR), fractional excretion of phosphate, renal expression of klotho, bone morphogenetic protein (BMP) 7 and superoxide dismutase. CONCLUSION Our data indicated that klotho supplementation reduced blood pressure and albuminuria with inactivation of renal RAS in the remnant kidney. In addition, exogenous klotho protein supplementation increased endogenous klotho expression, facilitating phosphate excretion with reductions in serum phosphate and FGF23. Finally, klotho protein supplementation upregulated BMP7, at least partly contributing to an increase in GFR and reversal of fibrosis in the remnant kidney.

Klotho supplementation attenuates blood pressure and albuminuria in murine model of IgA nephropathy.

Klotho interacts with various membrane proteins, such as transforming growth factor-β (TGFβ) and insulin-like growth factor (IGF) receptors. The renal expression of klotho is diminished in chronic kidney disease. In this study, we assessed the effects of klotho supplementation on a murine model of IgA nephropathy. Twenty-four-week-old hyper serum IgA (HIGA) mice were subcutaneously injected daily with recombinant human klotho protein (20 μg/kg per day) or the vehicle. After 2 months, the mice were killed using an anesthesia overdose and their kidneys were harvested for analysis. Supplementation of exogenous klotho protein reduced SBP, albuminuria, 8-epi-prostaglandin F2α excretion, glomerular filtration rate, renal angiotensin II concentration, and angiotensinogen expression in HIGA mice. Additionally, it enhanced renal expression of superoxide dismutase (SOD) and renal klotho itself. The findings using laser-manipulated microdissection demonstrated that klotho supplementation reduced the glomerular expression of TGFβ, fibronectin, and IGF, and increased the glomerular expression of connexin (Cx) 40. These results indicate that klotho supplementation reduces blood pressure by suppressing the renin--angiotensin system in HIGA mice. Klotho inhibits IGF signaling to preserve glomerular Cx40 levels, ameliorating albuminuria in HIGA mice. Klotho protein supplementation attenuates mesangial expansion by inhibiting TGFβ signaling in HIGA mice.

Dietary nitrate reduces blood pressure and cerebral artery velocity fluctuations and improves cerebral autoregulation in transient ischemic attack patients.

Accentuated blood pressure (BP) fluctuation and low cerebral blood flow (CBF) response to CO2 increase the risk of transient ischemic attack (TIA) recurrence and stroke in TIA patients. Improving cardio- and cerebrovascular function may reduce stroke risk. We found dietary nitrate lowered dynamic blood pressure variability (BPV) in rats and improved cerebrovascular CO2 reactivity in healthy individuals. In 30 TIA patients, we examined the effects of a 7-day supplementation of dietary nitrate (0.1 mmol·kg-1·day-1) on cerebrovascular function using a randomized, single-blinded, placebo-controlled study design. We hypothesized that 7-day dietary nitrate supplementation would decrease variabilities in BP and CBF and improve CBF-CO2 slope and cerebral autoregulation (CA). We assessed beat-to-beat middle cerebral artery blood velocity (MCAv; index of CBF) and BP at rest and during CO2 breathing. Transfer function analysis was performed on beat-to-beat MCAv and BP to determine CA parameters (gain, phase, and coherence). Irrespective of treatment, high- and low-frequency BP-MCAv gain and MCAv-CO2 slope increased 7 days following TIA onset, while low-frequency BPV decreased (P < 0.05 vs. baseline). At follow-up, dietary nitrate elevated plasma nitrate concentration by ~547% (P < 0.001) and moderately lowered BPV (d = 0.6, P = 0.011), MCAv variability (d = 0.7, P = 0.018), and BP-MCAv coherence (d = 0.7, P = 0.008) in the very-low-frequency range (0.02-0.07 Hz), while MCAv-CO2 slope and arterial stiffness were unaffected (P > 0.05). Concurrent with standard treatment, dietary nitrate supplementation reduces BP and CBF fluctuation and improves cerebral autoregulation in TIA patients, without affecting cerebrovascular CO2 reactivity.NEW & NOTEWORTHY We found dietary nitrate supplementation reduced blood pressure and brain blood flow fluctuations and improved the relationship between blood pressure and brain blood flow in transient ischemic attack patients. Meanwhile, dietary nitrate had no effects on the brain blood vessels' response to CO2. We attribute the improved brain blood flow stability to the improved myogenic control of blood pressure with dietary nitrate. Our findings indicate that dietary nitrate could be an effective strategy for stabilizing blood pressure and brain blood flow following transient ischemic attack.

Dietary nitrate does not alter cardiac function, calcium handling proteins, or SERCA activity in the left ventricle of healthy rats.

Dietary nitrate has been shown to increase cytosolic calcium concentrations within the heart, which would necessitate greater calcium sequestration for relaxation. In the present study we demonstrate that while nitrate supplementation reduced blood pressure, calcium-handling protein content, sarco(endo)plasmic reticulum Ca-ATPase 2a (SERCA) enzymatic properties, and left ventricular function were not altered. In addition, nitrite did not alter in vitro SERCA activity. Combined, these data suggest that in healthy rats, dietary nitrate does not increase left ventricle SERCA-related calcium-handling properties. Novelty Dietary nitrate decreases blood pressure but does not alter left ventricular calcium-handling protein content or SERCA activity in healthy rats.

Prenatal vitamin D supplementation reduces blood pressure and improves placental angiogenesis in an animal model of preeclampsia.

Preeclampsia (PE), a pregnancy complication, is characterized by abnormal placental angiogenesis. The current study examines the effect of vitamin D deficiency/supplementation on pregnancy outcome and placental angiogenesis using an animal model of PE. Pregnant Wistar rats were divided into four groups: Control; PE; Vitamin D deficient with PE (VDD-PE) and Vitamin D supplemented with PE (VDS-PE). PE was induced by administering l-nitroarginine methyl ester (l-NAME) at the dose of 50 mg per kg body weight per day from day 14 to day 19 gestation in all the 4 groups. During the pre-pregnancy and pregnancy period, the rats from the Control and PE groups were fed a control diet, the VDD-PE group received a vitamin D deficient diet and the VDS-PE group received a vitamin D supplemented diet. Dams were sacrificed at d20 of gestation. l-NAME administration increased systolic as well as diastolic blood pressure in both PE and VDD-PE groups as compared to the control (p < 0.01). Vitamin D supplementation was beneficial in reducing the blood pressure. Vitamin D deficiency also lowered the placental protein levels of pro-angiogenic proteins VEGF and Flt-1 (p < 0.05 and p < 0.01, respectively), while the levels of these proteins in the VDS-PE group were similar to those in the control group. Vitamin D status did not influence the levels of PlGF and Hif1α. A low dose vitamin D supplementation given from pre-pregnancy and throughout pregnancy was beneficial in reducing the blood pressure and normalizing the placental levels of VEGF and Flt-1. This has implications for reducing the severity of preeclampsia.

L-arginine supplementation reduces blood pressure and plasma lipid levels in an animal model of perimenopause induced by 4-Vinylcyclohexene diepoxide

The incidence of women developing high blood pressure during perimenopause has been documented and is sustained till menopause. However, no study till date on beneficial effects of L-arginine supplementation on BP during perimenopause in humans and animal models of perimenopause.Female rats 28 days old were divided into 3 groups; Control group was injected (SC) daily with Corn oil (2.5 μl/g BW) for 15 days, allowed to grow till 12th week; VCD group was injected (SC) daily with 4-vinylcyclohexene diepoxide (160 mg/kg BW) diluted in Corn oil (2.5 μl/g BW) for 15 days, allowed to grow till 12th week; VCD + L-ARG group was injected as VCD group, allowed to grow till 8th week, then administered oral 100mg/kg L-arginine daily for additional 4 weeks. Caudal BP was measured with tail-cuff apparatus (Kent Scientific CODA system) at weeks eight, ten, and twelve. Terminal BP was also measured with a power-lab apparatus and blood samples were subsequently collected for measurement of plasma lipid profile.L-arginine supplementation significantly reduced systolic, diastolic and mean arterial BP parameters in the VCD + L-ARG group compared to the Control and VCD groups (P < 0.05). It also significantly reduced total cholesterol and LDL concentrations in the VCD + L-ARG group compared to the Control and VCD groups (P < 0.05). HDL concentration was significantly higher in the VCD and VCD + L-ARG groups compared to the Control group (P < 0.05). These results show that L-arginine supplementation ameliorates some cardiovascular risk factors during perimenopausal transitory period.

Klotho protein supplementation reduces blood pressure and renal hypertrophy in db/db mice, a model of type 2 diabetes.

Klotho interacts with various membrane proteins, such as receptors for transforming growth factor (TGF)-β and insulin-like growth factor (IGF), to alter their function. Renal expression of klotho is diminished in diabetes. The present study examined whether exogenous klotho protein supplementation ameliorates kidney injury and renin-angiotensin system (RAS) in db/db mice. We investigated the effects of klotho supplementation on diabetic kidney injury and RAS. Recombinant human klotho protein (10μg/kg/d) was administered to db/db mice daily. Klotho protein supplementation reduced kidney weight, systolic blood pressure (SBP), albuminuria, glomerular filtration rate, and 8-epi-prostaglandin F2α excretion without affecting body weight. Although klotho supplementation did not alter glycated albumin, it reduced renal angiotensin II levels associated with reduced renal expression of angiotensinogen. Klotho supplementation improved renal expression of superoxide dismutase (SOD), and endogenous renal expression of klotho. Klotho supplementation reduced the levels of hypoxia-inducible factor, phosphorylated Akt, and phosphorylated mTOR and decreased the renal expression of TGF-β, tumour necrosis factor (TNF), and fibronectin. These data indicate that klotho supplementation reduces blood pressure and albuminuria along with ameliorating renal RAS activation in db/db mice. Furthermore, these results suggest that klotho inhibits IGF signalling, induces SOD expression to reduce oxidative stress, and suppresses Akt-mTOR signalling to inhibit abnormal kidney growth. Collectively, the results suggest that klotho inhibits TGF-β and TNF signalling, resulting in a decline in renal fibrosis.

Chronic 17Beta‐Estradiol Supplementation Reduces Blood Pressure and Alters Renal Estrogen Receptor Expression in Female Growth‐Restricted Rats in Later Life

The role of estrogen in mediating protective cardiovascular (CV) effects in menopausal women is controversial. The prevalence of hypertension in women born low birth weight is two‐fold greater at the age of 60 relative to normal birth weight women. In addition, low birth weight women exhibit increased adiposity by middle‐age and an earlier age at menopause. In our model of intrauterine growth restriction (IUGR) induced by placental insufficiency in the pregnant rat, female IUGR offspring have an elevated blood pressure (BP) at 12 months of age that is associated with increased adiposity. Female IUGR also exhibit reproductive senescence by 12 months of age, or 6 months prior to female control, resulting in a shift in the estradiol to testosterone ratio. To determine the importance of estradiol on the CV profile in female IUGR, we tested the hypothesis that chronic 17Beta‐estradiol (E2) supplementation would reduce BP and alter the renal expression of the nuclear estrogen receptors, alpha (ER‐alpha) and beta (ER‐beta). Placebo or E2 pellets (1.5 mg 17Beta‐estradiol, 60‐day release) were initiated at 12 months of age for 6 weeks followed by measurement of BP in conscious, chronically catheterized animals and collection of kidneys for molecular analysis. Real‐time PCR was used to measure renal mRNA expression of ER‐alpha and ER‐beta; Western blot was used to measure ER‐Alpha protein expression. BP was significantly decreased in E2‐treated IUGR relative to placebo‐treated IUGR (decrease of 13 mmHg, P&lt;0.05), whereas BP was not significantly altered in E2‐treated control relative to placebo‐treated control (increase of 2 mmHg). Preliminary studies suggest that cortical ER‐alpha mRNA expression did not differ in placebo‐treated IUGR versus placebo‐treated control. Yet, medullary ER‐alpha mRNA expression was decreased in placebo‐treated IUGR versus placebo‐treated control, but not in E2‐treated IUGR. Preliminary studies also reveal that cortical ER‐beta mRNA expression was increased 4‐fold in placebo‐treated IUGR versus placebo‐treated control. However, cortical ER‐beta mRNA expression was not increased in E2‐treated IUGR counterparts. Cortical and medullary ER‐alpha protein expression did not differ in IUGR versus control, or E2‐treated versus placebo‐treated groups. The CV protective effects attributed to estrogen include: vasodilation via nitric oxide production, angiogenesis, and modulation of components of the renin angiotensin system (RAS). Therefore, alterations in BP in female IUGR vs. female control may be attributed to changes in the expression of ERs with future studies investigating the effect of E2 on the RAS which is up‐regulated in female IUGR at 12 months of age. To conclude, although a loss of female sex hormones may not be the only contributing factor to increases in BP after menopause in LBW women, therapies that target specific estrogen receptors may prove beneficial in improving cardiovascular health.Support or Funding InformationHL074927, AHAGRNT19900004 (Alexander), HL51971, P20GM104357 (Hall), T32HL105324 (Granger), F30DK112718 (Newsome)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Omega-3 polyunsaturated fatty acid supplementation reduces blood pressure but not renal vasoconstrictor response to orthostatic stress in healthy older adults.

Older adults exhibit augmented renal vasoconstriction during orthostatic stress compared to young adults. Consumption of omega‐3 polyunsaturated fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) found in fish oil (FO), modulates autonomic nerve activity. However, the effect of omega‐3 polyunsaturated fatty acid consumption on the renal vasoconstrictor response to orthostatic stress in young and older adults is unknown. Therefore, 10 young (25 ± 1 years; mean ± SEM) and 10 older (66 ± 2 years) healthy adults ingested 4 g FO daily for 12 weeks, and underwent graded lower body negative pressure (LBNP; −15 and −30 mmHg) pre‐ and post‐FO supplementation. Renal blood flow velocity (RBFV; Doppler ultrasound), arterial blood pressure (BP; photoplethysmographic finger cuff), and heart rate (electrocardiogram) were recorded. Renal vascular resistance (RVR), an index of renal vasoconstriction, was calculated as mean BP/RBFV. All baseline cardiovascular values were similar between groups and visits, except diastolic BP was higher in the older group (P < 0.05). FO supplementation increased erythrocyte EPA and DHA content in both groups (P < 0.05). FO did not affect RVR or RBFV responses to LBNP in either group, but attenuated the mean BP response to LBNP in the older group (older −30 mmHg: pre‐FO −4 ± 1 vs. post‐FO 0 ± 1 mmHg, P < 0.05; young −30 mmHg: pre‐FO −5 ± 1 vs. post‐FO −5 ± 2 mmHg). In conclusion, FO supplementation attenuates the mean BP response but does not affect the renal vasoconstrictor response to orthostatic stress in older adults.

Effect of Calcitriol Supplementation on Blood Pressure in Older Adults

ABSTRACTRecent studies suggest that vitamin D plays an important role in the control of blood pressure. Unfortunately, because older adults are more likely to have low 25-hydroxyvitamin-D [25(OH)D] levels, this study investigated whether calcitriol supplementation reduces blood pressure in older adults with hypertension. The design was a double-blind placebo-controlled randomized clinical trial with 36 randomly assigned subjects (71.7 ± 10 years). Blood pressure and serum levels of 25(OH)D before and after calcitriol intervention (1,000 IU daily for 6 weeks; n = 22) or placebo (n = 23) for 6 weeks were analyzed. At the end of the study, the calcitriol group presented a significant decrease of systolic blood pressure [20.25 mmHg (p = 0.001)] and diastolic blood pressure [7 mmHg (p = 0.01)], compared with the placebo group. In conclusion, 1,000 IU/day of calcitriol for 6 weeks efficiently reduced systolic and diastolic blood pressure levels in this population of older adults presenting with high blood pressure (Clinical Trial Approbation NCT02047799).

Dietary Supplementation Of Ca++, K+ And No-3 Upon Blood Pressure And Exercise In Pre-Hypertension Patients

Dietary supplementations of Ca++, K+, NO3- and acute exercise, produce significant post-exercise hypotension in healthy normotensive subjects. However this nutritional approach and its effects have not been investigated in adults with prehypertension or hypertension. PURPOSE: to examine the effect of dietary supplementation Ca++, K+, NO-3 and maximal exercise in adults with pre or hypertension. METHODS: Sixty five subjects (49 men and 16 women aged 44±4 yr) participated in this study. None had absolute contraindications for a maximal exercise test (maxcap-t). Subjects arrived at 8:00 in fasting conditions without medications for at least 72 hrs. After 10 minutes of sitting rest, blood pressure (BP) was measured twice to verify the diagnosis of prehypertension or hypertension. Patients were admitted if BP was ≥ 120/80 mmHg. Immediately after inclusion, they ingested a sandwich and juice of fruit and vegetables containing 900 mg of Ca++, 3500 mg of K+ (~90% of RDA) and 254 gr (8 mmo/L) of nitrate. BP was measured: 10 minutes post arrival, 90 min postDS, immediately after maxcap-t , 10 min after maxcap-t and 150 min after maxcap-t. RESULTS:Table 1: Blood pressure at rest and after DT and Maxcap-t.* P < 0.05 vs BP control. Values are mean±SD of SBP/DBP. Both SBP and DBP decreased 3±5/3±4 mmHg at 90 min postDS. SBP increased 22±16/2±8 mmHg and DBP did not change. There was a significant reduction in both BP 11±11/8±7 mmHg at 4 hours postDS (150 min post maxcap-t). CONCLUSIONS: Combined cations-anions and nitrate supplementation reduced blood pressure at rest and after maximal endurance exercise in middle-aged adults with prehypertension or hypertension.

Effects of dietary polyphenols on metabolic syndrome features in humans: a systematic review

Dietary polyphenols constitute a large family of bioactive substances potential beneficial effect on metabolic syndrome (MetS). This review summarizes the results of clinical studies on patients with MetS involving the chronic supplementation of a polyphenol-rich diet, foods, extracts or with single phenolics on the features of MetS (obesity, dyslipidemia, blood pressure and glycaemia) and associated complications (oxidative stress and inflammation). Polyphenols were shown to be efficient, especially at higher doses, and there were no specific foods or extracts able to alleviate all the features of MetS. Green tea, however, significantly reduced body mass index and waist circumference and improved lipid metabolism. Cocoa supplementation reduced blood pressure and blood glucose. Soy isoflavones, citrus products, hesperidin and quercetin improved lipid metabolism, whereas cinnamon reduced blood glucose. In numerous clinical studies, antioxidative and anti-inflammatory effects were not significant after polyphenol supplementation in patients with MetS. However, some trials pointed towards an improvement of endothelial function in patients supplemented with cocoa, anthocyanin-rich berries, hesperidin or resveratrol. Therefore, diets rich in polyphenols, such as the Mediterranean diet, which promote the consumption of diverse polyphenol-rich products could be an effective nutritional strategy to improve the health of patients with MetS. © 2016 The Authors. Obesity Reviews published by John Wiley & Sons Ltd on behalf of World Obesity.

Garlic and Heart Disease

Background: Thousands of studies have been published based on animal and human studies evaluating garlic’s effects and safety.Objective: We reviewed the available literature investigating the effects of garlic supplements on hypertension, hypercholesterolemia, C-reactive protein (CRP), pulse wave velocity (PWV), and coronary artery calcium (CAC), as well as available data on side effects.Methods: We searched PubMed for all human studies using medical subject heading words through 30 May 2013 and assessed relevant review articles and original studies. Only double-blind, randomized, controlled trials and meta-analyses of double-blind, randomized, controlled trials were included. The review of articles and data extraction were performed by 2 independent authors, with any disagreements resolved by consensus.Results: Garlic supplementation reduced blood pressure by 7–16 mm Hg (systolic) and 5–9 mm Hg (diastolic) (4 meta-analyses and 2 original studies). It reduced total cholesterol by 7.4–29.8 mg/dL (8 meta-analyses). The most consistent benefits were shown in studies that used aged garlic extract (AGE). A few small studies that used AGE also showed favorable effects on CAC, CRP, and PWV. Although garlic is generally safe, rare adverse reactions have been documented with limited causality established.Conclusion: We conclude that garlic supplementation has the potential for cardiovascular protection based on risk factor reduction (hypertension and total cholesterol) and surrogate markers (CRP, PWV, and CAC) of atherosclerosis. Larger studies are warranted to evaluate these effects further.

Augmented reflex cutaneous vasodilatation following short-term dietary nitrate supplementation in humans.

What is the central question of this study? Nitrate supplementation via beetroot juice has been shown to have several benefits in healthy humans, including reduced blood pressure and increased blood flow to exercising muscle. Whether nitrate supplementation can improve blood flow to the skin in heat-stressed humans has not been investigated. What is the main finding and its importance? Similar to previous studies, we found that nitrate supplementation reduces blood pressure. Nitrate supplementation increased vasodilatation in the skin of heat-stressed humans but did not directly increase skin blood flow. Nitrate supplementation has been shown to increase NO-dependent vasodilatation through both NO synthase (NOS)-dependent and NOS-independent pathways. We hypothesized that nitrate supplementation would augment reflex cutaneous active vasodilatation. Subjects were equipped with two microdialysis fibres on the forearm randomly assigned as control (Ringer solution) or NOS inhibition (20mm l-NAME). Whole-body heating was performed to raise core temperature by 0.8°C above baseline core temperature. Maximal cutaneous vasodilatation was achieved via 54mm sodium nitroprusside and local heating to 43°C. Skin blood flow (measured by laser-Doppler flowmetry) and blood pressure were measured. Cutaneous vascular conductance (CVC) was calculated as skin blood flow divided by mean arterial pressure (MAP) and expressed as a percentage of maximal CVC (%CVCmax ). Subjects underwent heat stress before and after nitrate supplementation (3days of beetroot juice; 5mm, 0.45g nitrates per day). During heat stress, MAP was reduced following nitrate supplementation compared with the control conditions (before 88±3mmHg versus after 78±2mmHg; P<0.05); however, resting MAP was not different between conditions (before 88±3mmHg versus after 83±2mmHg; P=0.117). Nitrate supplementation increased plateau CVC at control sites (before 67±2%CVCmax versus after 80±5%CVCmax ; P=0.01) but not at l-NAME-treated sites (before 45±4%CVCmax versus after 40±5%CVCmax ; P=0.617). There was no change in the calculated percentage of NOS-dependent vasodilatation before and after supplementation (before 59±4%versus after 64±6%; P=0.577). These data suggest that nitrate supplementation augments CVC and reduces MAP during heat stress.

Chia flour supplementation reduces blood pressure in hypertensive subjects.

The aim of this study was to investigate the effect of chia supplementation (Salvia hispanica L.) on blood pressure (BP) and its associated cardiometabolic factors in treated and untreated hypertensive individuals. The subjects were randomly assigned to one of the following groups: the hypertensive-drug treated (CHIA-MD, n = 10), hypertensive untreated (CHIA-NM, n = 9) and placebo (PLA-MD, n = 7) groups. The subjects consumed 35 g/day of either chia flour or a placebo for 12 weeks. The clinical and ambulatory BP, inflammation, oxidative stress and markers for nitric oxide were measured. While the PLA-MD group showed no changes in BP, there was a reduction in the mean clinical blood pressure (MBP) in the CHIA (111.5 ± 1.9 to 102.7 ± 1.5 mmHg, p < 0.001) and CHIA-MD (111.3 ± 2.2 to 100.1 ± 1.8 mmHg, p < 0.001) groups. The CHIA-NM group showed no reduction in the MBP but did show a decreased systolic BP (146.8 ± 3.8 to 137.3 ± 3.1 mmHg, p < 0.05). The clinical BP reduction was demonstrated by a 24 h ambulatory systolic reduction in all of the supplemented groups. However, the mean ambulatory BP was reduced only in the CHIA (98.1 ± 2.4 to 92.8 ± 2.2 mmHg, p < 0.05) group, and there was no change in the diastolic component in either of the CHIA groups. The lipid peroxidation was reduced in the CHIA (p = 0.04) and CHIA-NM (p = 0.02) groups compared with the PLA-MD group. A reduction in the plasma nitrite levels was observed only in the CHIA group (p = 0.02). Chia flour has the ability to reduce ambulatory and clinical BP in both treated and untreated hypertensive individuals.

Coconut oil supplementation reduces blood pressure and oxidative stress in spontaneously hypertensive rats

Coconut oil supplementation reduces blood pressure and oxidative stress in spontaneously hypertensive rats

Abstract 292: Vitamin D Supplementation Reduces CD4+ T Cells, Blood Pressure and Autoantibodies to the AT1 Receptor (AT1-AA) in a Rat Model of Preeclampsia

Preeclampsia (PE) is characterized by the development of hypertension, endothelial dysfunction and chronic immune activation after 20 weeks of gestation. PE women exhibit elevated CD4 + T cells, proinflammatory cytokines and agonistic autoantibodies to the angiotensin II type I receptor (AT1-AA). Vitamin D deficiency is associated with increased prevalence of hypertension and chronic inflammatory diseases both in the presence and absence of pregnancy. We utilize the Reduced Uterine Perfusion Pressure (RUPP) model of PE in the pregnant rat which exhibits hypertension, endothelial dysfunction as well as increased CD4 + T cells, inflammatory cytokines and AT1-AA. Therefore, we tested the hypothesis that administration of exogenous Vitamin D2 (VD2) and Vitamin D3 (VD3) would ameliorate hypertension and or chronic inflammation associated with placental ischemia in the RUPP rat. For these studies, the RUPP procedure was performed on gestation day 14 (GD14) and normal pregnant (NP) and RUPP rats were treated daily with 50uM VD2 or VD3 via oral gavage on GD14-18. Carotid catheters were inserted on GD18 and blood pressure (MAP), blood and tissues were collected on GD19. Flow cytometry was used to evaluate CD4 + T cells in control RUPP rats and RUPP rats treated with Vitamin D. On GD19, MAP was increased in RUPP rats to 123 ± 3.5 compared to 108.8 ± 4.3 mmHg in NP rats (n=5-6, p&lt;0.05). Supplementation with either VD2 or VD3 lowered MAP to 113 ± 6.9 or 115.4 ± 2.3 mmHg, respectively (n=4-5). CD4 + T cells in RUPP compared to NP rats increased from 2.80 ± 0.95 to 8.49 ± 1.52 percent (n=8-11, p&lt;0.05). Circulating CD4 + T cells fell to 1.22 ± 0.41 percent with VD2 and to 4.59 ± 3.67 percent with VD3 (n=2-3). AT1-AA levels, measured via chronotropic response in cardiomyocytes, were 19.50 ± 0.44 beats/min in RUPP rats and decreased to 15.35 ± 0.69 with VD3, and further to 8.33 ± 0.51 with VD2 supplementation (n=5, p&lt;0.05). Taken together, these data indicate that pharmaceutical Vitamin D supplementation reduced blood pressure and markers of chronic inflammation in a rat model of PE, thereby suggesting a role for Vitamin D supplementation to improve hypertension and chronic inflammation in response to diseases associated with placental ischemia, such as PE.

Taurine supplementation reduces blood pressure and prevents endothelial dysfunction and oxidative stress in post-weaning protein-restricted rats.

IntroductionTaurine is a sulfur-containing amino acid that exerts protective effects on vascular function and structure in several models of cardiovascular diseases through its antioxidant and anti-inflammatory properties. Early protein malnutrition reprograms the cardiovascular system and is linked to hypertension in adulthood. This study assessed the effects of taurine supplementation in vascular alterations induced by protein restriction in post-weaning rats.Methods and ResultsWeaned male Wistar rats were fed normal- (12%, NP) or low-protein (6%, LP) diets for 90 days. Half of the NP and LP rats concomitantly received 2.5% taurine supplementation in the drinking water (NPT and LPT, respectively). LP rats showed elevated systolic, diastolic and mean arterial blood pressure versus NP rats; taurine supplementation partially prevented this increase. There was a reduced relaxation response to acetylcholine in isolated thoracic aortic rings from the LP group that was reversed by superoxide dismutase (SOD) or apocynin incubation. Protein expression of p47phox NADPH oxidase subunit was enhanced, whereas extracellular (EC)-SOD and endothelial nitric oxide synthase phosphorylation at Ser 1177 (p-eNOS) were reduced in aortas from LP rats. Furthermore, ROS production was enhanced while acetylcholine-induced NO release was reduced in aortas from the LP group. Taurine supplementation improved the relaxation response to acetylcholine and eNOS-derived NO production, increased EC-SOD and p-eNOS protein expression, as well as reduced ROS generation and p47phox expression in the aortas from LPT rats. LP rats showed an increased aortic wall/lumen ratio and taurine prevented this remodeling through a reduction in wall media thickness.ConclusionOur data indicate a protective role of taurine supplementation on the high blood pressure, endothelial dysfunction and vascular remodeling induced by post-weaning protein restriction. The beneficial vascular effect of taurine was associated with restoration of vascular redox homeostasis and improvement of NO bioavailability.