Ascorbic acid does not affect large elastic artery compliance or central blood pressure in young and older men

Large elastic artery compliance is reduced and arterial blood pressure (BP) is increased in the central (cardiothoracic) circulation with aging. Reactive oxygen species may tonically modulate central arterial compliance and BP in humans, and oxidative stress may contribute to adverse changes with aging. If so, antioxidant administration may have beneficial effects. Young (Y; 26 ± 1 yr, mean ± SE) and older (O; 63 ± 2 yr, mean ± SE) healthy men were studied at baseline and during acute (intravenous infusion; Y: n = 13, O: n = 12) and chronic (500 mg/day for 30 days; Y: n = 10, O: n = 10) administration of ascorbic acid (vitamin C). At baseline, peripheral (brachial artery) BP did not differ in the two groups, but carotid artery compliance was 43% lower (1.2 ± 0.1 vs. 2.1 ± 0.1 mm2/mmHg × 10–1, P < 0.01) and central (carotid) BP (systolic: 116 ± 5 vs. 101 ± 3 mmHg, P < 0.05, and pulse pressure: 43 ± 4 vs. 36 ± 3 mmHg, P = 0.16), carotid augmentation index (AIx; 27.8 ± 7.8 vs. –20.0 ± 6.6%, P < 0.001), and aortic pulse wave velocity (PWV; 950 ± 88 vs. 640 ± 38 cm/s, P < 0.01) were higher in the older men. Plasma ascorbic acid concentrations did not differ at baseline (Y: 71 ± 5 vs. O: 61 ± 7 μmol/l, P = 0.23), increased ( P < 0.001) to supraphysiological levels during infusion (Y: 1,240 ± 57 and O: 1,056 ± 83 μmol/l), and were slightly elevated ( P < 0.001 vs. baseline) with supplementation (Y: 96 ± 5 μmol/l vs. O: 85 ± 6). Neither ascorbic acid infusion nor supplementation affected peripheral BP, heart rate, carotid artery compliance, central BP, carotid AIx, or aortic PWV (all P > 0.26). These results indicate that the adverse changes in large elastic artery compliance and central BP with aging in healthy men are not 1) mediated by ascorbic acid-sensitive oxidative stress (infusion experiments) and 2) affected by short-term, moderate daily ascorbic acid (vitamin C) supplementation.

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Ascorbic acid increases cardiovagal baroreflex sensitivity in healthy older men

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01054.2003 ◽

2004 ◽

Vol 286 (6) ◽

pp. H2113-H2117 ◽

Cited By ~ 43

Author(s):

Kevin D. Monahan ◽

Iratxe Eskurza ◽

Douglas R. Seals

Keyword(s):

Oxidative Stress ◽

Blood Pressure ◽

Ascorbic Acid ◽

Systolic Blood Pressure ◽

Sodium Nitroprusside ◽

Baroreflex Sensitivity ◽

Older Men ◽

Acid Infusion ◽

Healthy Men ◽

Phenylephrine Hydrochloride

Cardiovagal baroreflex sensitivity (BRS) declines with advancing age in healthy men. We tested the hypothesis that oxidative stress contributes mechanistically to this age-associated reduction. Eight young (23 ± 1 yrs, means ± SE) and seven older (63 ± 3) healthy men were studied. Cardiovagal BRS was assessed using the modified Oxford technique (bolus infusion of 50–100 μg sodium nitroprusside, followed 60 s later by a 100- to 150-μg bolus of phenylephrine hydrochloride) in triplicate at baseline and during acute intravenous ascorbic acid infusion. At baseline, cardiovagal BRS (slope of the linear portion of the R-R interval-systolic blood pressure relation during pharmacological changes in arterial blood pressure) was 56% lower ( P < 0.01) in older (8.3 ± 1.6 ms/mmHg) compared with young (19.0 ± 3.1 ms/mmHg) men. Ascorbic acid infusion increased plasma concentrations similarly in young (62 ± 9 vs. 1,249 ± 72 μmol/l for baseline and during ascorbic acid; P < 0.05) and older men (62 ± 4 vs. 1,022 ± 55 μmol/l; P < 0.05) without affecting baseline blood pressure, heart rate, carotid artery compliance, or the magnitude of change in systolic blood pressure in response to bolus sodium nitroprusside and phenylephrine hydrochloride infusion. Ascorbic acid (vitamin C) infusion increased cardiovagal BRS in older (Δ58 ± 16%; P < 0.01), but not younger (Δ − 4 ± 4%) men. These data provide experimental support for the concept that oxidative stress contributes mechanistically to age-associated reductions in cardiovagal BRS in healthy men.

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Oxidative stress-induced dysregulation of arteriolar wall shear stress and blood pressure in hyperhomocysteinemia is prevented by chronic vitamin C treatment

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00448.2003 ◽

2003 ◽

Vol 285 (6) ◽

pp. H2277-H2283 ◽

Cited By ~ 34

Author(s):

Zsolt Bagi ◽

Csongor Csekö ◽

Erika Tóth ◽

Akos Koller

Keyword(s):

Oxidative Stress ◽

Blood Pressure ◽

Shear Stress ◽

Wall Shear Stress ◽

Vitamin C ◽

Arterial Blood ◽

Control Serum ◽

Arteriolar Wall ◽

Wall Shear

We aimed to test the hypothesis that an enhanced level of reactive oxygen species (ROS) is primarily responsible for the impairment of nitric oxide (NO)-mediated regulation of arteriolar wall shear stress (WSS) in hyperhomocysteinemia (HHcy). Thus flow/WSS-induced dilations of pressurized gracilis muscle arterioles (basal diameter: ∼170 μm) isolated from control (serum Hcy: 6 ± 1 μM), methionine diet-induced HHcy rats (4 wk, serum Hcy: 30 ± 6 μM), and HHcy rats treated with vitamin C, a known antioxidant (4 wk, 150 mg · kg body wt–1 · day–1; serum Hcy: 32 ± 10 μM), were investigated. In vessels of HHcy rats, increases in intraluminal flow/WSS-induced dilations were converted to constrictions. Constrictions were unaffected by inhibition of NO synthesis by Nω-nitro-l-arginine methyl ester (l-NAME). Vitamin C treatment of HHcy rats reversed the WSS-induced arteriolar constrictions to l-NAME-sensitive dilations but did not affect control responses. Similar changes in responses were obtained for the calcium ionophore A-23187. In addition, diastolic and mean arterial blood pressure and serum 8-isoprostane levels (a marker of in vivo oxidative stress) were significantly elevated in rats with HHcy, changes that were normalized by vitamin C treatment. Taken together, our data show that in chronic HHcy long-term vitamin C treatment, by decreasing oxidative stress in vivo, enhanced NO bioavailability, restored the regulation of shear stress in arterioles, and normalized systemic blood pressure. Thus our study provides evidence that oxidative stress is an important in vivo mechanism that is primarily responsible for the development of endothelial dysregulation of WSS in HHcy.

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The Lipophilic Vitamin C Derivative, 6-O-Palmitoylascorbate Protects Human Keratinocytes and 3D-Human Skin Equivalents Against X-Ray-Induced Oxidative Stress and Apoptosis More Markedly Than L-Ascorbic Acid

Journal of Cellular Biochemistry ◽

10.1002/jcb.25639 ◽

2016 ◽

Vol 118 (2) ◽

pp. 318-329 ◽

Cited By ~ 3

Author(s):

Li Xiao ◽

Nobuhiko Miwa

Keyword(s):

Oxidative Stress ◽

Ascorbic Acid ◽

Vitamin C ◽

Human Skin ◽

Human Keratinocytes ◽

X Ray ◽

Skin Equivalents

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Vitamin C supplementation improves blood pressure and oxidative stress after acute exercise in patients with poorly controlled type 2 diabetes mellitus: A randomized, placebo-controlled, cross-over study

The Chinese Journal of Physiology ◽

10.4103/cjp.cjp_95_20 ◽

2021 ◽

Vol 64 (1) ◽

pp. 16

Author(s):

Naruemon Leelayuwat ◽

Chongchira Boonthongkaew ◽

Terdthai Tong-Un ◽

Yupaporn Kanpetta ◽

Nisa Chaungchot ◽

...

Keyword(s):

Oxidative Stress ◽

Diabetes Mellitus ◽

Blood Pressure ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Vitamin C ◽

Acute Exercise ◽

Vitamin C Supplementation ◽

And Oxidative Stress

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Abstract P105: Greater 24 Hour Blood Pressure Variability is Associated With Higher 24 Hour Systolic Blood Pressure and Glucose Independent of Age and Large Elastic Artery Stiffness in Normotensive Adults

Hypertension ◽

10.1161/hyp.68.suppl_1.p105 ◽

2016 ◽

Vol 68 (suppl_1) ◽

Author(s):

Lyndsey E DuBose ◽

Seth W Holwerda ◽

Amy K Stroud ◽

Nealy A Wooldridge ◽

Janie E Myers ◽

...

Keyword(s):

Blood Pressure ◽

Risk Factor ◽

Blood Glucose ◽

Carotid Artery ◽

Linear Regression ◽

Fasting Blood Glucose ◽

Large Artery ◽

Stepwise Linear Regression ◽

Artery Stiffness ◽

Elastic Artery

Older age is associated with elevated large elastic artery stiffness, a strong predictor of cardiovascular (CVD) risk in middle-age/older (MA/O) adults independent of blood pressure (BP). Greater 24-hour systolic BP variability (BPV) is also an independent risk factor for CVD and is linked to large artery stiffness in MA/O adults with hypertension and diabetes. However, its relation to age-related arterial stiffness in adults with low risk factor burden is unclear. We hypothesized that higher systolic BPV would be: 1) associated with advancing age, and 2) related to elevated aortic and carotid artery stiffness among healthy MA/O adults. To determine this, 98 healthy adults (ages 19-70 yrs) with measurements of systolic BPV (standard deviation of 24 hr systolic BP) via ambulatory BP monitoring, aortic stiffness (carotid-femoral pulse wave velocity, cfPWV), carotid artery stiffness (β-stiffness via carotid tonometry/B mode ultrasound) and circulating metabolic factors were included. In the entire cohort, greater systolic BPV was not associated with age, cfPWV, carotid β stiffness or circulating lipids/glucose (all P>0.05), but was correlated (age-adjusted) with 24 hr systolic BP (r= 0.41, P<0.001) and BMI (r= 0.21, P<0.05). In stepwise linear regression analyses that included age, sex, BMI, only 24 hr systolic BP was associated with systolic BPV (β= 0.14 ± 0.03, Model R 2 = 0.20, P< 0.001). Interestingly, there was no difference in 24 hr systolic BPV (11.4 ± 0.4 vs 11.4 ± 0.5 SD mmHg, P=0.99) in young (n=55; 29.0 ± 0.7 yrs) vs. MA/O (n= 43; 53.0 ± 1.2 yrs) adults despite higher cfPWV (594 ± 12 vs 913 ± 39 cm/sec, P<0.001), carotid β-stiffness (6.8 ± 0.6 vs 9.3 ±0.9 U, P=0.001) and 24 hr systolic BP (121 ± 1 vs 125 ± 2 mmHg, P<0.05). Systolic BPV was associated with BMI (r= 0.42, p< 0.01) and fasting blood glucose (r= 0.54, P= 0.001) in MA/O but not young adults. In a stepwise linear regression model among MA/O, 24 hr systolic BP (β= 0.18 ± 0.04, R 2 = 0.36, P<0.001) and fasting glucose (β= 0.10 ± 0.05, R 2 change= 0.07, P<0.001) were the only significant correlates of systolic BPV (Model R 2 = 0.43, P<0.001). In conclusion, 24 hr systolic BP and fasting blood glucose, but not age or large elastic artery stiffness, were the strongest determinants of higher systolic BPV in normotensive MA/O adults.

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Peripheral chemoreflex activation and cardiac function during hypoxemia in near term fetal sheep without placental compromise

Journal of Applied Physiology ◽

10.1152/japplphysiol.01111.2020 ◽

2021 ◽

Author(s):

Juulia Lantto ◽

Tiina Erkinaro ◽

Mervi Haapsamo ◽

Heikki Huhta ◽

Leena Alanne ◽

...

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Carotid Artery ◽

Arterial Oxygen ◽

Sheep Model ◽

Fetal Sheep ◽

Descending Aorta ◽

Arterial Blood ◽

Near Term ◽

Peripheral Chemoreflex

A drop in arterial oxygen content activates fetal chemoreflex including an increase in sympathetic activity leading to peripheral vasoconstriction and redistribution of blood flow to protect the brain, myocardium, and adrenal glands. By using a chronically instrumented fetal sheep model with intact placental circulation at near-term gestation, we investigated the relationship between peripheral chemoreflex activation induced by hypoxemia and central hemodynamics. 17 Åland landrace sheep fetuses at 115-128/145 gestational days were instrumented. Carotid artery was catheterised in 10 fetuses and descending aorta in 7 fetuses. After a 4-day recovery, baseline measurements of fetal arterial blood pressures, blood gas values, and fetal cardiovascular hemodynamics by pulsed Doppler ultrasonography were obtained under isoflurane-anesthesia. Comparable data to baseline was collected 10 (acute hypoxemia) and 60 minutes (prolonged hypoxemia) after maternal hypo-oxygenation to saturation level of 70-80% was achieved. During prolonged hypoxemia, pH and base excess (BE) were lower, and lactate levels higher in the descending aorta than in the carotid artery. During hypoxemia mean arterial blood pressure (MAP) in the descending aorta increased, while in the carotid artery MAP decreased. In addition, right pulmonary artery pulsatility index values increased, and the diastolic component in the aortic isthmus blood flow velocity waveform became more retrograde. Both fetal ventricular cardiac outputs were maintained even during prolonged hypoxemia when significant fetal metabolic acidemia developed. Fetal chemoreflex activation induced by hypoxemia decreased the perfusion pressure in the cerebral circulation. Fetal weight-indexed LVCO or AoI Net Flow-ratio did not correlate with a drop in carotid artery blood pressure.

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Moderate zinc restriction during fetal and postnatal growth of rats: effects on adult arterial blood pressure and kidney

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00050.2008 ◽

2008 ◽

Vol 295 (2) ◽

pp. R543-R549 ◽

Cited By ~ 48

Author(s):

Analía Lorena Tomat ◽

Felipe Inserra ◽

Luciana Veiras ◽

María Constanza Vallone ◽

Ana María Balaszczuk ◽

...

Keyword(s):

Oxidative Stress ◽

Blood Pressure ◽

Lipid Peroxidation ◽

Systolic Blood Pressure ◽

Zinc Deficiency ◽

Control Diet ◽

Adult Life ◽

Fetal Life ◽

Arterial Blood ◽

End Products

Intrauterine and postnatal zinc restriction may result in an adverse environment for the development of cardiovascular and renal systems. This study evaluated the effects of moderate zinc deficiency during fetal life, lactation, and/or postweaning growth on systolic blood pressure, renal function, and morphology in adult life. Female Wistar rats received low (8 ppm) or control (30 ppm) zinc diets from the beginning of pregnancy up to weaning. After weaning, male offspring of each group of mothers were fed low or control zinc diet. Systolic blood pressure, creatinine clearance, proteinuria, renal morphology, renal apoptosis. and renal oxidative stress state were evaluated after 60 days. Zinc deficiency during pre- and postweaning growth induced an increase in systolic blood pressure and a decrease in the glomerular filtration rate associated with a reduction in the number and size of nephrons. Activation of renal apoptosis, reduction in catalase activity, glutathione peroxidase activity, and glutathione levels and increase in lipid peroxidation end products could explain these morphometric changes. Zinc deficiency through pre- and postweaning growth induced more pronounced renal alteration than postweaning zinc deficiency. These animals showed signs of renal fibrosis, proteinuria, increased renal apoptosis, and higher lipid peroxidation end products. A control diet during postweaning growth did not totally overcome renal oxidative stress damage, apoptosis, and fibrosis induced by zinc deficiency before weaning. In conclusion, zinc deficiency during a critical period of renal development and maturation could induce functional and morphological alterations that result in elevated blood pressure and renal dysfunction in adult life.

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