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

2008 ◽  
Vol 295 (2) ◽  
pp. R543-R549 ◽  
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.

scholarly journals Aging increases Oxidative Stress and Renal Expression of Oxidant and Antioxidant Enzymes that Are Associated with an Increased Trend in Systolic Blood Pressure

2009 ◽  
Vol 2 (3) ◽  
pp. 138-145 ◽  
Author(s):  
Pedro Gomes ◽  
Sónia Simão ◽  
Elisabete Silva ◽  
Vanda Pinto ◽  
João S. Amaral ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Lipid Peroxidation ◽  
Renal Function ◽  
Antioxidant Enzymes ◽  
Systolic Blood Pressure ◽  
Renal Cortex ◽  
Antioxidant Defenses ◽  
Wky Rats ◽  
Old Rats

The aim of this study was to investigate whether the effects of aging on oxidative stress markers and expression of major oxidant and antioxidant enzymes associate with impairment of renal function and increases in blood pressure. To explore this, we determined age-associated changes in lipid peroxidation (urinary malondialdehyde), plasma and urinary hydrogen peroxide (H2O2) levels, as well as renal H2O2production, and the expression of oxidant and antioxidant enzymes in young (13 weeks) and old (52 weeks) male Wistar Kyoto (WKY) rats. Urinary lipid peroxidation levels and H2O2production by the renal cortex and medulla of old rats were higher than their young counterparts. This was accompanied by overexpression of NADPH oxidase components Nox4 and p22phoxin the renal cortex of old rats. Similarly, expression of superoxide dismutase (SOD) isoforms 2 and 3 and catalase were increased in the renal cortex from old rats. Renal function parameters (creatinine clearance and fractional excretion of sodium), diastolic blood pressure and heart rate were not affected by aging, although slight increases in systolic blood pressure were observed during this 52-week period. It is concluded that overexpression of renal Nox4 and p22phoxand the increases in renal H2O2levels in aged WKY does not associate with renal functional impairment or marked increases in blood pressure. It is hypothesized that lack of oxidative stress-associated effects in aged WKY rats may result from increases in antioxidant defenses that counteract the damaging effects of H2O2.

Morphological and functional effects on cardiac tissue induced by moderate zinc deficiency during prenatal and postnatal life in male and female rats

2013 ◽  
Vol 305 (11) ◽  
pp. H1574-H1583 ◽  
Author(s):  
Analia Lorena Tomat ◽  
Lorena Vanesa Juriol ◽  
María Natalia Gobetto ◽  
Luciana Cecilia Veiras ◽  
Facundo Mendes Garrido Abregú ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Left Ventricle ◽  
Zinc Deficiency ◽  
Adult Life ◽  
Female Rats ◽  
Postnatal Life ◽  
Fetal Life ◽  
Male And Female ◽  
Cardiac Morphology ◽  
And Function

The aim of this study was to evaluate whether moderate zinc restriction in rats throughout fetal life, lactation, and/or postweaning growth results in early changes in cardiac morphology predisposing the onset of cardiac dysfunction in adult life as well as sex-related differences in the adaptation to this nutritional injury. Female Wistar rats received low or control zinc diets from the beginning of pregnancy up to offspring weaning. After being weaned, offspring were fed either a low or control zinc diet until 81 days. Systolic blood pressure was measured. Echocardiographic and electrocardiographic examinations, morphological experiments, and apoptosis by TUNEL assay were performed in the left ventricle. In the early stages, zinc-deficient male and female offspring showed an increase in cardiomyocyte diameter, probably associated with an increase in cardiac apoptotic cells, but smaller myocyte diameters in adulthood. In adult males, this nutritional injury induced decreased contractility and dilatation of the left ventricle, not allowing the heart to compensate the higher levels of blood pressure, and hypertrophic remodeling of coronary arteries associated with increased blood pressure. Adequate zinc intake during postweaning life did not overcome blood pressure levels but reversed some of the detrimental effects of earlier zinc deficiency in cardiac morphology and function. Females were less sensitive to this deficiency, exhibiting normal levels of blood pressure and no structural or functional heart alterations in adult life. The present study demonstrates that the effects of zinc deficiency on blood pressure, cardiac morphology, and function differ between sexes, with males more predisposed to develop cardiovascular diseases in adulthood.

scholarly journals A METHOD TO DETERMINE THE PERIPHERAL ARTERIAL BLOOD PRESSURE IN THE MOUSE

1941 ◽  
Vol 74 (1) ◽  
pp. 29-40 ◽  
Author(s):  
Philip D. McMaster
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Arterial Blood Pressure ◽  
Close Agreement ◽  
Carotid Arteries ◽  
Systolic Pressure ◽  
Arterial Blood ◽  
Relative Transparency ◽  
Direct Measurements ◽  
Peripheral Arterial

Advantage has been taken of the relative transparency of the claw of the mouse to devise a method, here described, to measure the blood pressure in the animal's leg. Direct measurements of the systolic blood pressure from the carotid arteries of anesthetized mice have also been made. Simultaneous blood pressure readings by both these methods applied to the same animal showed close agreement. The systolic pressure ranged from 60 to 126 mm. Hg, according to the conditions.

Proximal tubule microvilli remodeling and albuminuria in the Ren2 transgenic rat

2007 ◽  
Vol 292 (2) ◽  
pp. F861-F867 ◽  
Author(s):  
Melvin R. Hayden ◽  
Nazif A. Chowdhury ◽  
Shawna A. Cooper ◽  
Adam Whaley-Connell ◽  
Javad Habibi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Proximal Tubule ◽  
Structural Damage ◽  
Kidney Tissue ◽  
Proximal Tubule Cell ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

TG(mRen2)27 (Ren2) transgenic rats overexpress the mouse renin gene, with subsequent elevated tissue ANG II, hypertension, and nephropathy. The proximal tubule cell (PTC) is responsible for the reabsorption of 5–8 g of glomerular filtered albumin each day. Excess filtered albumin may contribute to PTC damage and tubulointerstitial disease. This investigation examined the role of ANG II-induced oxidative stress in PTC structural remodeling: whether such changes could be modified with in vivo treatment with ANG type 1 receptor (AT1R) blockade (valsartan) or SOD/catalase mimetic (tempol). Male Ren2 (6–7 wk old) and age-matched Sprague-Dawley rats were treated with valsartan (30 mg/kg), tempol (1 mmol/l), or placebo for 3 wk. Systolic blood pressure, albuminuria, N-acetyl-β-d-glucosaminidase, and kidney tissue malondialdehyde (MDA) were measured, and ×60,000 transmission electron microscopy images were used to assess PTC microvilli structure. There were significant differences in systolic blood pressure, albuminuria, lipid peroxidation (MDA and nitrotyrosine staining), and PTC structure in Ren2 vs. Sprague-Dawley rats (each P < 0.05). Increased mean diameter of PTC microvilli in the placebo-treated Ren2 rats ( P < 0.05) correlated strongly with albuminuria ( r2 = 0.83) and moderately with MDA ( r2 = 0.49), and there was an increase in the ratio of abnormal forms of microvilli in placebo-treated Ren2 rats compared with Sprague-Dawley control rats ( P < 0.05). AT1R blockade, but not tempol treatment, abrogated albuminuria and N-acetyl-β-d-glucosaminidase; both therapies corrected abnormalities in oxidative stress and PTC microvilli remodeling. These data indicate that PTC structural damage in the Ren2 rat is related to the oxidative stress response to ANG II and/or albuminuria.

Abstract P489: Effect of Continuous Intake of Hesperidin on Blood Pressure in 2-kidney, 1-clip Renovasucular Hypertensive Rats

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Ayuna Yamaoka ◽  
Yukiko Segawa ◽  
Saki Maruyama ◽  
Natsumi Saito ◽  
Hiroko Hashimoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mrna Expression ◽  
Control Diet ◽  
Left Renal Artery ◽  
Sham Operation ◽  
Hypertensive Rats ◽  
Fruit Peel ◽  
Arterial Blood ◽  
Significant Difference ◽  
Enos Mrna

Objective: Hesperidin (HES) is a flavonoid which is contained in citrus fruit peel. It has physiological effects on blood vessels such as strengthening capillary vessels. Thus, it is known to be one of the effective ingredients of herbal medicine. Some studies have shown that the intake of HES decreases blood pressure (BP) in spontaneously hypertensive rats. The antihypertensive effect of HES is suggested to be due to vasodilation by nitric oxide (NO). However, its mechanism has not been clarified in detail. In this study, we observed whether HES intake decreases BP in 2-kidney, 1-clip renovasucular hypertensive rats (2K1C) and evaluated endothelial NO synthase (eNOS) mRNA to investigate its role in the mechanism. Methods: Male Sprague-Dawley rats (6 weeks old) were treated with sham operation (SHAM) or clipping the left renal artery (2K1C). After surgery, the rats started receiving continuously a control diet (C) or a diet containing 0.1% (w/w) HES for 6 weeks. The systolic BP (SBP) was measured by a tail-cuff method every week. At the end of the protocol, mean arterial blood pressure (MAP) was measured in each rat under anesthesia. Then, the aortas were removed for extracting mRNA. eNOS mRNA expression was evaluated using real-time RT-PCR. Results: At the end of the protocol, SBP in 2K1C-C was significantly higher than in SHAM-C (170±6 vs 117±6 mmHg, p <0.001). On the other hand, 2K1C-HES was lower in SBP (141±4 mmHg) than 2K1C-C ( p <0.01). There were no significant differences between SHAM-HES (122±7 mmHg) and SHAM-C. MAP at the end of the protocol were similar to in SBP. ANOVA revealed mRNA expression of eNOS was significantly higher in 2K1C than in SHAM ( p <0.05), and showed no significant difference between C and HES, nor a significant interaction. Conclusion: Continuous intake of HES may suppress BP increase in 2K1C. The role of eNOS mRNA expression may not be involved in the mechanism.

Maternal Carbenoxolone Treatment Lowers Birthweight and Induces Hypertension in the Offspring of Rats Fed a Protein-Replete Diet

1997 ◽  
Vol 93 (5) ◽  
pp. 423-429 ◽  
Author(s):  
Simon C. Langley-Evans
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Fetal Growth ◽  
Low Birthweight ◽  
Control Diet ◽  
Later Life ◽  
Hydroxysteroid Dehydrogenase ◽  
Fetal Exposure ◽  
Low Protein ◽  
Protein Diets

1. In the rat low birthweight and raised systolic blood pressure are the consequence of fetal exposure to maternal low protein diets. Nutritional down-regulation of the placental isoform of 11β-hydroxysteroid dehydrogenase, which may increase exposure of the fetus to maternal glucocorticoids, has been suggested to underlie effects of low protein diets on fetal growth and blood pressure. 2. Pregnant rats were fed control (18% casein) or low protein (9% casein) diets throughout gestation. Animals fed the control diet were injected with carbenoxolone, an inhibitor of 11β-hydroxysteroid dehydrogenase. Injections were administered either throughout pregnancy (days 0–22), or targeted to specific periods in early (days 0–7), mid- (days 8–14) or late (days 15–22) gestation. 3. Exposure to a low protein diet reduced birthweight and at 4 weeks of age systolic blood pressure was significantly elevated in the rats exposed to low protein. These hypertensive animals had small kidneys in proportion to body weight. 4. Fetal exposure to carbenoxolone at any period in gestation resulted in lower weight at birth. In rats exposed to the inhibitor over days 8–14, 15–22 or 0–22 systolic blood pressure at 4 weeks was significantly higher than in control animals. The greatest elevation of pressure was associated with carbenoxolone treatment in late (days 15–22) gestation. Animals with carbenoxolone-induced hypertension did not exhibit evidence of retarded renal growth. 5. Increased fetal exposure to maternal glucocorticoids impairs fetal growth and programmes elevated blood pressure in later life.

scholarly journals Acute Hemodynamic Changes Associated with Zumba and ZOCA Dance Exercises among Females of Selected Gyms in Lusaka, Zambia

2020 ◽  
Vol 2 (1) ◽  
pp. 84-91
Author(s):  
Chanda Grace Chisunka ◽  
◽  
Gibson Sijumbila ◽  
Fastone Goma ◽  
◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Systolic Blood Pressure ◽  
Hemodynamic Changes ◽  
Aerobic Dance ◽  
Arterial Blood ◽  
Effective Dynamic ◽  
Blood Pressure Monitors ◽  
Blood Pressures

Background: Dynamic exercises are known to elicit hemodynamic changes such as an increase in arterial blood pressure and heart rate. Zumba and ZOCA are part of a fast growing group of dance fitness programmes designed to provide a cardiovascular dynamic workout. Despite their growing popularity, very few studies have been done to provide knowledge regarding the hemodynamic changes associated with these exercises. Methods: Case study in which 27 females took part in either a Zumba or ZOCA class. Using digital blood pressure monitors, recordings of blood pressure and heart rate were taken, firstly, before commencement of the exercise, secondly, after 30 minutes after exercise and thirdly, at the end of the class.Results: Mean baseline blood pressures were 118 (SD = 14) mmHg and 77 (SD = 7) mmHg, systolic and diastolic blood pressures, respectively. After 30 minutes of dancing, mean systolic blood pressure increased to 130 (SD = 19) mmHg (p˂ 0.05) while diastolic blood pressureonly rose to an average of 80 (SD = 8) mmHg (p˃ 0.05). At the end of the class (after the cool down phase) mean systolic blood pressure reduced to 109 (SD = 13) mmHg (p˂0.05) while diastolic blood pressure reduced to 74(SD = 12) mmHg (p˂ 0.05). Conclusions: Zumba and ZOCA elicited significant hemodynamic changes that can be attributed to these exercises stimulating the cardiovascular regulatory mechanisms (e.g central command and exercise-pressor) sufficiently and hence resulting in autonomic adjustmentsthat were concurrent with effective dynamic exercise. Keywords: Blood Pressure, Heart Rate, Aerobic, Dance Exercise

scholarly journals Gut Microbiome-Derived Metabolite Trimethylamine N-Oxide Induces Aortic Stiffening and Increases Systolic Blood Pressure With Aging in Mice and Humans

Hypertension ◽  
2021 ◽  
Author(s):  
Vienna E. Brunt ◽  
Abigail G. Casso ◽  
Rachel A. Gioscia-Ryan ◽  
Zachary J. Sapinsley ◽  
Brian P. Ziemba ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Advanced Glycation End Products ◽  
Gut Microbiome ◽  
Disease Risk ◽  
Advanced Glycation ◽  
Wall Stiffness ◽  
Glycation End Products ◽  
End Products ◽  
Aortic Stiffening

Aging is associated with stiffening of the large elastic arteries and consequent increases in systolic blood pressure (SBP), which together increase cardiovascular disease risk; however, the upstream mechanisms are incompletely understood. Using complementary translational approaches in mice and humans, we investigated the role of the gut microbiome-derived metabolite trimethylamine N-oxide (TMAO) in age-related aortic stiffening and increased SBP. Aortic stiffness was measured using carotid-femoral or aortic pulse wave velocity (PWV) in humans and mice, respectively. Study 1: Plasma TMAO concentrations were elevated ( P <0.001) in healthy middle-aged to older (6.3±5.8 µmol/L) versus young (1.8±1.4 µmol/L) humans and positively related to carotid-femoral PWV ( r 2 =0.15, P <0.0001) and SBP ( r 2 =0.09, P <0.001), independent of traditional cardiovascular risk factors. Study 2: Dietary supplementation with TMAO increased aPWV in young mice and exacerbated the already elevated aPWV of old mice, accompanied by increases in SBP of ≈10 mm Hg in both groups. TMAO-supplemented versus control-fed mice also had higher intrinsic mechanical stiffness of the aorta (stress-strain testing) associated with higher aortic abundance of advanced glycation end-products, which form crosslinks between structural proteins to promote aortic stiffening. Study 3: Ex vivo incubation of aortic rings with TMAO increased intrinsic stiffness, which was attenuated by the advanced glycation end-products crosslink breaker alagebrium and prevented by inhibition of superoxide signaling. TMAO induces aortic stiffening and increases SBP via formation of advanced glycation end-products and superoxide-stimulated oxidative stress, which together increase intrinsic wall stiffness. Increases in circulating TMAO with aging represent a novel therapeutic target for reducing risk of aortic stiffening-related clinical disorders.

Abstract P246: Relationship Between Urinary Sodium/potassium Ratio And Systolic Blood Pressure In Salt Sensitive Subjects In The Dash-sodium Trial

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Rozalia Abramov ◽  
Elizabeth D Drugge ◽  
Khalid A Farhan ◽  
Nicholas R Ferreri
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Salt Intake ◽  
Control Diet ◽  
Dietary Sodium ◽  
Bivariate Analysis ◽  
Linear Regression Models ◽  
Unequal Distribution ◽  
Dash Diet ◽  
Black Females

Excessive salt intake is associated with hypertension and cardiovascular morbidity. However, identifying those at risk of salt sensitive hypertension (SSH) remains a challenge due to its unequal distribution among populations and inaccurate assessment of dietary sodium (Na) and potassium (K) intake. The objective of this study was to compare indices of dietary Na intake in relation to systolic blood pressure (SBP) in salt sensitive (SS) and salt resistant (SR) subjects from the Dietary Approaches to Stop Hypertension (DASH)-Sodium trial. We hypothesized that when compared to urinary Na or K independently, Na/K ratio is a better predictor of SSH when defined as a 5-10 mmHg change in SBP from low to high dietary Na. Among 404 Black and White subjects, baseline classifications included 177 SS and 227 SR. After diet randomization, on the control 107 were SS and 92 SR and on the DASH 70 were SS and 135 SR. Descriptive statistics, bivariate analysis, followed by linear regression models for baseline and multilevel mixed-effects models after intervention were used to assess the relationship between SBP and dietary Na (as measured by urinary Na/K ratio or Na and K independently) using SS as a categorical factor. SBP was consistently associated with SS, Na/K ratio, and age in all models . At baseline, SBP was significantly higher in SS and SR subjects of the same race and sex, after controlling for age and urinary Na/K ratio and was highest for White females, SS:142.3 (138.8, 145.7) vs. SR:133.2 (130.7, 135.7), and for Black males, SS:137.0 (133.8, 140.1) vs. SR: 129.6 (127.0, 132.3). On average, SBP increased 1.02 (0.065, 1.98) mmHg with each unit increase in Na/K ratio and 3.30 (2.41, 4.19) mmHg with each 10-year increase in age. After randomization and exposure to increasing levels of sodium, SBP increased in SS subjects on the control diet:125.3 (123.2, 127.3) to 136.8 (134.8, 138.9), an effect that was greater in White vs Black females and in Black vs White males. SBP increased in SS subjects on the DASH diet: 121.4 (118.8, 124.0) to 131.2 (128.7, 133.7), but there were no differences by race and sex. These results suggest that a 5-10 mmHg change in SBP in subjects on a typical American diet and Na/K ratio are good predictors of SSH and that the DASH diet may help to reduce race and sex disparities.

Mechanisms of vascular instability in a transgenic mouse model of sickle cell disease

2000 ◽  
Vol 279 (6) ◽  
pp. R1949-R1955 ◽  
Author(s):  
K. A. Nath ◽  
V. Shah ◽  
J. J. Haggard ◽  
A. J. Croatt ◽  
L. A. Smith ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Lipid Peroxidation ◽  
Sickle Cell Disease ◽  
Mouse Model ◽  
Systolic Blood Pressure ◽  
Transgenic Mouse ◽  
Sickle Cell ◽  
Transgenic Mouse Model ◽  
Cell Disease

We investigated a transgenic mouse model of sickle cell disease, homozygous for deletion of mouse β-globin and containing transgenes for human βSand βS-antillesglobins linked to the transgene for human α-globin. In these mice, basal cGMP production in aortic rings is increased, whereas relaxation to an endothelium-dependent vasodilator, A-23187, is impaired. In contrast, aortic expression of endothelial nitric oxide synthase (NOS) is unaltered in sickle mice, whereas expression of inducible NOS is not detected in either group; plasma nitrate/nitrite concentrations and NOS activity are similar in both groups. Increased cGMP may reflect the stimulatory effect of peroxides (an activator of guanylate cyclase), because lipid peroxidation is increased in aortae and in plasma in sickle mice. Despite increased vascular cGMP levels in sickle mice, conscious systolic blood pressure is comparable to that of aged-matched controls; sickle mice, however, evince a greater rise in systolic blood pressure in response to nitro-l-arginine methyl ester, an inhibitor of NOS. Systemic concentrations of the vasoconstrictive oxidative product 8-isoprostane are increased in sickle mice. We conclude that vascular responses are altered in this transgenic sickle mouse and are accompanied by increased lipid peroxidation and production of cGMP; we suggest that oxidant-inducible vasoconstrictor systems such as isoprostanes may oppose nitric oxide-dependent and nitric oxide-independent mechanisms of vasodilatation in this transgenic sickle mouse. Destabilization of the vasoactive balance in the sickle vasculature by clinically relevant states may predispose to vasoocclusive disease.

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