Hypertension In Adult Life Research Articles

Epigenetic changes to the carotid body drive hypertension in perinatal nicotine exposed rats

Background: Epigenetic changes can be shaped by a wide array of environmental cues as well as maternal health and behaviors. One of the most detrimental behaviors to the developing fetus is nicotine exposure. Perinatal nicotine exposure remains as a significant risk factor for cardiovascular health and in particular, hypertension, as it has been shown to alter angiotensin signaling. Hypothesis: We hypothesized that perinatal nicotine exposure alters carotid body angiotensin signaling to induce hypertension in adult life. Methods: Pregnant Sprague-Dawley rats were exposed to nicotine (2mg/kg SQ, or PBS- control) from estrous day 6 to post-natal day (PND) 21. Experiments on pups took place from PND 56-90. Carotid bodies were harvested pooled together for RNAseq and confirmation of unbiased transcriptomics was conducted with qPCR. Blood pressure was measured with indwelling telemetry. ELISA assessed serum angiotensin. PC12 cells were used a surrogate for carotid body glomus cells and were used for calcium imaging. Results: Unbiased RNAseq of carotid bodies from nicotine exposed pups compared to saline control pups showed that KEGG pathways with significant angiotensin signaling components including Neuroactive ligand-receptor interaction (Log2FC=2.4, p=7.5x10−8) and Dopaminergic synapse (Log2FC=2.3, p=0.0007) were significantly upregulated. qPCR of carotid bodies demonstrated that Angiotensin II type 1 receptor (56%↑), Angiotensin II type 2 receptor (15%↑) and TRPV1 channels (63%↑) were upregulated in nicotine exposed pups compared to controls. Blood pressure measured in nicotine exposed pups was suppressed 1 day after bilateral carotid body denervation. Circulating angiotensin assessed from serum was similar between nicotine exposed and control pups. Calcium imaging of PC12 cells showed that nicotine significantly increased spike frequency in response to nicotine (0.2mg/ml). Incubation with nicotine + Angiotensin (50ng/ml) did not further increase spike frequency. This increased excitation was suppressed with losartan (3μM), AMG9810 (TRPV1 antagonist, 10μM) and combined blockade (p<0.05). Conclusion: Our data demonstrate that adverse maternal behaviors produce epigenetic changes to carotid bodies of offspring resulting in neurogenic hypertension. The epigenetic changes involve an Angiotensin-Angiotensin II type 1 receptor-TRPV1 channel axis in the carotid body without any significant systemic changes. We suggest carotid body modulation may have a significant health impact on offspring with adverse perinatal environmental exposures. UCOP TRDRP T32IP4707, T32KT4708. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Birth weight and hypertension: nature or nurture?

Birth weight and hypertension: nature or nurture?

Association of Early Sports Practice with Cardiovascular Risk Factors in Community-Dwelling Adults: A Retrospective Epidemiological Study

BackgroundSports practice in childhood and adolescence has been inversely related to the chances of developing cardiovascular risk factors (CRFs). However, it is not clear whether sports practice in childhood and adolescence could be inversely related to CRF in adult life.ObjectivesThis study aimed to analyze the association between early sports practice and cardiovascular risk factors in a randomized sample of community-dwelling adults.MethodsFor this, 265 adults aged ≥ 18 years composed the sample. Cardiovascular risk factors of obesity, central obesity, diabetes, dyslipidemia, and hypertension were collected. Early sports practice was retrospectively self-reported using an appropriate instrument. Total physical activity level was assessed by accelerometry. The association between early sports practice and cardiovascular risk factors in adulthood was analyzed by binary logistic regression, adjusted for sex, age, socioeconomic status, and moderate-to-vigorous physical activity.ResultsEarly sports practice was observed in 56.2% of the sample. The prevalence of central obesity (31.5 vs. 50.0%; p = 0.003), diabetes (4.7% vs. 13.7%; p = 0.014), dyslipidemia (10.7% vs. 24.1%; p = 0.005), and hypertension (14.1% vs. 34.5%; p = 0.001) was lower in participants who reported early sports practice. Participants who reported early sports practice in childhood and adolescence were, respectively, 60% (OR = 0.40; 95% CI 0.19–0.82) and 59% (OR = 0.41; 95% CI 0.21–0.82) less likely to have hypertension in adult life when compared to those with no early sports practice, independently of sex, age, socioeconomic status, and habitual physical activity level in adulthood.ConclusionEarly sports practice in childhood and adolescence was a protective factor for hypertension in adulthood.

Diet and Weight Management in Adolescent Girls.

Dietary behaviors established in adolescence usually lead to long-term health consequences. Consuming foods high in fat and sugar on one side and adopting sedentary lifestyle on the other side are responsible for overweight and obesity in adolescent girls which increases the risk of diabetes and hypertension in adult life. Meal convenience is important to many adolescents. In the bargain, they may eat too much of wrong types of food. Teenagers should be taught about the five healthy groups i.e., Grains, proteins, vegetables, fruits and dairy products. Food items with different colors, textures and tastes, both fresh and cooked should be included at every meal and for snacks. The healthiest and the cheapest drink is nothing else but clean water. Adolescent girls need iron-rich food to compensate for monthly period blood loss. Adolescence is not a good time for crash diets as girls will not get enough nutrients to reach their full potential.

Association of Placental Weight With Birth Weight, Gestational Age, and Risk Factors Related to Maternal Morbidity, Diet, Activity, and Rest

Background: Placental weight and its relationship to infant size at birth have been studied for more than a century.[1] A low placental weight is associated with the medical complications in the mother.[2] The risk of essential hypertension in adult life falls with increasing birth weight and rises with increasing placental weight and that the mothers at highest risk are those with a high placental weight relative to birth weight-that is, a high placental ratio.[3] Aims/Objective: To study association of placental weight with birth weight, gestational age and maternal morbidity, diet, activity and rest. Settings and Design / Methods and Material: A cohort of 1876 apparently healthy pregnant women registered and attending antenatal clinic of Krishna Hospital was studied to find out the correlation of the placental weight with the LBW and preterm births and their association with selected maternal risk factors. Statistical Analysis Used: Correlation (r), Chi-square test, Analysis of Variance (ANOVA) and Boneferroni test, Unpaired 't' test, were used. Results: There was a statistically significant association of the mean placental weight with the mean birth weight and proportion of LBW of the baby as indicated by ANOVA test. (F= 29.627; p<0.001) and (χ2 =102.6; p<0.001) respectively. There was a statistically significant association of the mean placental weight with the mean gestational period of the baby and proportion of the preterm births as indicated by ANOVA test. (F= 7.694; p<0.001) and (χ2=18.377;p<0.001) respectively. Daily frequency of meals < 4, antenatal morbidity of preeclampsia, PIH and APH were associated with lesser placental weight. Conclusion: There was a significant association of placental weight with birth weight, gestational age, maternal morbidity and frequency of maternal meals.

Medical and obstetric factors associated with preterm deliveries among women of childbearing age at Pumwani maternity hospital, Nairobi County, Kenya

Background: The rate of pre-term birth (PTB) in Kenya stands at 12.3%. Preterm deliveries are associated with high neonatal mortality and have a huge financial burden on the parents and the government. Prematurity is also associated with chronic diseases like diabetes and hypertension in adult life. The study objective was to determine the medical1and obstetric factors1associated1with preterm deliveries among women of childbearing age (15-49 years) at Pumwani maternity hospital (PMH).Methods: A hospital-based cross-sectional study was conducted among 191 mothers of reproductive age (15-49 years) who delivered at PMH during the study period. Data was collected using a questionnaire and a data abstraction tool. Descriptive statistics were used to summarize categorical variables. Chi-square was used to test for the strengths of associations. Prevalence adjusted odds ratios (PAOR) were used to estimate the strengths of associations.Results: The study found that the association between past pregnancy (p=1.0), history of surgery (p=1.0), medication (p=1.0), urinary tract infection (p=0.453), miscarriage (p=1.0) and chronic disease (p=0.395) and preterm delivery among women of child bearing age (15-49 years) at PMH was not statistically significant. The association between premature delivery (p=0.021), parity (p=0.000), premature rapture of membranes (PROM) (p=0.000), antepartum hemorrhage (APH) (p=0.045), cervical incompetence (p=0.001), pre-eclampsia toxemia (PET) (p=0.000), and placenta abruption complications (p=0.009) and preterm delivery was statistically significant.Conclusions: The association between premature delivery, parity, PROM, APH, cervical incompetence, PET and placenta abruption complications and preterm delivery was statistically significant.

The reliance on α-adrenergic receptor stimuli for blood pressure regulation in the chronically hypoxaemic fetus is not dependent on post-ganglionic activation.

Chronic hypoxaemia is associated with intrauterine growth restriction (IUGR) and a predisposition to the development of hypertension in adult life. IUGR fetuses exhibit a greater reliance on α-adrenergic activation for blood pressure regulation. The fetal blood pressure response to post-ganglionic blockade is not different between control and IUGR fetuses. The decrease in mean arterial pressure is greater in the IUGR sheep fetus after α-adrenergic receptor blockade at the level of the vasculature and this is inversely related to fetal . The increased reliance that the IUGR fetus has on α-adrenergic activation for maintenance of mean arterial pressure is not a result of increased post-ganglionic sympathetic activation. Intrauterine growth restriction (IUGR) is associated with an increased risk of cardiovascular disease in adult life. Placental restriction (PR) in sheep results in chronic hypoxaemia and early onset IUGR with increased circulating plasma noradrenaline concentrations. These IUGR fetuses exhibit a greater decrease in mean arterial pressure (MAP) during α-adrenergic blockade. We aimed to determine the role of post-ganglionic sympathetic activation with respect to regulating MAP in IUGR fetal sheep. PR was induced by carunclectomy surgery prior to conception. Fetal vascular catheterization was performed at 110-126days gestational age (GA) (term, 150 days) in nine control and seven PR-IUGR fetuses. The fetal blood pressure response to both a post-ganglionic and an α-adrenergic receptor blocker was assessed at 116-120days GA and/or 129-131days GA. The effect of both post ganglionic and α-adrenergic blockade on fetal blood pressure was then compared between control and IUGR fetuses at both GAs. There was no difference in the effect of post-ganglionic blockade on MAP in control and IUGR fetal sheep at either 116-120days GA or 129-131days GA. α-adrenergic receptor blockade decreased MAP to the same extent in both control and IUGR fetuses at 116-120days GA. At 129-131days GA, the drop in MAP in response to α-adrenergic receptor blockade was greater in IUGR fetuses than controls. There was a significant inverse relationship between the drop in MAP in response to α-adrenergic receptor blockade at both GAs with fetal . Thus, the increased dependence on α-adrenergic activation for blood pressure regulation in the chronically hypoxaemic IUGR fetus is not a result of increased post-ganglionic sympathetic activation.

The Malaria-High Blood Pressure Hypothesis: Revisited.

Malaria etiologies with pathophysiological similarities to hypertension currently constitute a major subject of research. The malaria-high blood pressure hypothesis is strongly supported by observations of the increasing incidence of hypertension in malaria-endemic, low- and middle-income countries with poor socioeconomic conditions, particularly in sub-Saharan African countries. Malnutrition and low birth weight with persistent symptomatic malaria presentations in pregnancy correlate strongly with the development of preeclampsia, gestational hypertension and subsequent hypertension in adult life. Evidence suggest that the link between malaria infection and high blood pressure involves interactions between malaria parasites and erythrocytes, the inflammatory process, effects of the infection during pregnancy; effects on renal and vascular functions as well as effects in sickle cell disease. Possible mechanisms which provide justification for the malaria-high blood pressure hypothesis include the following: endothelial dysfunction (reduced nitric oxide (NO) levels), impaired release of local neurotransmitters and cytokines, decrease in vascular smooth muscle cell viability and/or alterations in cellular calcium signaling leading to enhanced vascular reactivity, remodeling, and cardiomyopathies, deranged homeostasis through dehydration, elevated intracellular mediators and proinflammatory cytokine responses, possible genetic regulations, activation of the renin-angiotensin-aldosterone system mechanisms and renal derangements, severe anemia and hemolysis, renal failure, and end organ damage. Two key mediators of the malaria-high blood pressure association are: endothelial dysfunction (reduced NO) and increased angiotensin-converting enzyme activity/angiotensin II levels. Sickle cell disease is associated with protection against malaria infection and reduced blood pressure. In this review, we present the state of knowledge about the malaria-blood pressure hypothesis and suggest insights for future studies.

Pathogenic role of angiotensin II and the NF-κB system in a model of malignant hypertensive nephrosclerosis

We previously reported that rats treated with an NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC), during lactation developed hypertension in adult life, without apparent functional or structural damage to kidneys, providing a new model of essential hypertension. Here, we investigated whether uninephrectomy associated with salt overload would unveil a latent renal dysfunction in this model, aggravating arterial hypertension and promoting renal injury. Male Munich-Wistar rat pups received PDTC from maternal milk (PDTCLact) from 0 to 20 days after birth. Another group received no treatment during lactation. All offspring underwent uninephrectomy (UNx) at 10 weeks of age and then were subdivided into NS, receiving a normal salt (0.5% Na+) diet, PDTCLact + NS, HS, receiving a high-salt diet (2% Na+ chow + 0.5% saline to drink), and PDTCLact+HS. Twelve weeks later, HS rats were moderately hypertensive with mild albuminuria and renal injury. In contrast, severe hypertension, glomerulosclerosis, and cortical collagen deposition were prominent in PDTCLact + HS animals, along with "onion-skin" arteriolar lesions, evidence of oxidative stress and intense renal infiltration by macrophages, and lymphocytes and angiotensin II-positive cells, contrasting with low circulating renin. The NF-κB pathway was also activated. In a separate set of PDTCLact+HS rats, Losartan treatment prevented NF-κB activation and strongly attenuated glomerular injury, cortical fibrosis, and renal inflammation. NF-κB activity during late nephrogenesis is essential for the kidneys to properly maintain sodium homeostasis in adult life. Paradoxically, this same system contributed to renal injury resembling that caused by malignant hypertension when renal dysfunction caused by its inhibition during lactation was unmasked by uninephrectomy associated with HS.

Prevalence of Primary Hypertension and Risk Factors in Grade XII Learners in KwaZulu-Natal, South Africa.

Hypertension in childhood leads to hypertension in adult life, the strongest risk factor being obesity. This study determined the prevalence of primary hypertension and its risk factors in Grade XII learners in KwaZulu-Natal, South Africa, from March 2016 to June 2017. Weight, height, body mass index (BMI), random finger prick cholesterol and glucose, and spot urine for an albumin : creatinine ratio were measured. An average of three separate blood pressure readings taken was at least 5 minutes apart. Five hundred and sixty-four learners had weight, height, and BMI; 536 had random blood glucose; and 545 had cholesterol and random spot urine albumin : creatinine ratios measured. Prehypertension was detected in 168 (29.7%) and hypertension in 77 (13.7%) of learners. Ninety (15.9%) were overweight and 75 (13,3%) were obese. Hypercholesterolaemia was present in 58 (10.8%) and a high spot random urine albumin : creatinine ratio in 5 (1.0%). None had a high blood glucose level. Both prehypertension and hypertension in all learners showed a significant increase with increasing BMI. Six (1.0%) learners had metabolic syndrome. Female learners in other racial groups (defined as Indian, mixed race, and White learners), overweight, and obese learners showed significantly higher rates of hypercholesterolaemia. We showed overweight and obesity as risk factors for prehypertension and hypertension. This presages the need for an appropriate diet and adequate exercise in a child's school career.

Does Low Birthweight Have an Impact on Living Kidney Donor Outcomes?

IntroductionBecause nearly 30,000 people worldwide become living kidney donors each year, donor safety is of the utmost importance. Recent studies have shown that living kidney donation is associated with an increased relative risk for end-stage renal disease (ESRD). It is essential to determine which donors will be more likely to develop ESRD. One of the risk factors for ESRD in living kidney donors is hypertension and, because there are studies demonstrating that low birthweight is a risk factor for developing hypertension in adult life, we hypothesized that donors with low birthweight may be at higher risk of developing renal disease after donation. MethodsSeventy-three living kidney donors were examined. Donors were divided into 2 cohorts: a group with low birthweight and group with normal birthweight. We checked whether the donor birthweight has an impact on the outcome of donor renal function and on the development of hypertension. ResultsHypertension was observed statistically more frequent in the group with low birthweight (P = .003). ConclusionGlomerular filtration rate before kidney donation was found to be lower in the low-birthweight group.

Abstract 003: Growth Trajectories of Body Mass Index During Childhood and Adult Hypertension

Background: Childhood body mass index (BMI) predicts adult hypertension. However, information is lacking regarding the relationship between BMI growth trajectories during childhood and adult hypertension risk. We aimed to test the hypothesis that BMI growth rates at different childhood ages have differential influences on adult hypertension risk, independent of BMI levels. Methods: The study included 1,772 Whites and 960 Blacks with repeated BMI and blood pressure measurements from childhood (4-19 years) to adulthood (20-51 years). A random-effects mixed model was used to construct BMI growth curves by race and sex. Model-estimated linear growth rates of BMI at different childhood ages were linked to adult hypertension (defined by measured blood pressure or antihypertensive medication) in multivariable logistic regression models. Results: Hypertensive adults had higher BMI across childhood than normotensive adults. Overall, linear slope and cubic parameters of BMI were higher in hypertensive adults than in normotensive adults in all four race-sex groups (p ≤ 0.023). Odds ratio of adult hypertension for each kg/m 2 /year increase in BMI linear slope was 1.22 (95% CI =1.11-1.34) at age 4, was non-significant between ages 5-9, and gradually increased thereafter and plateaued beginning at age 15 (odds ratio = 1.41 and 95% CI = 1.28-1.56) (Figure). Conclusions: Rapid increase in BMI during and after puberty is associated with elevated risk of hypertension in adult life, which has implications for early prevention.

Chronic Hypertension in Women after Perinatal Exposure to Preeclampsia, Being Born Small for Gestational Age or Preterm.

There is an established association between adverse events during perinatal life and chronic hypertension in adult life. However, disadvantageous conditions often co-exist in the same pregnancy. We investigated single and joint perinatal exposure to preeclampsia, being born small for gestational age (SGA) or preterm and subsequent risk of chronic hypertension. The study population consisted of 731 008 primiparous women from Norway and Sweden registered in the Medical Birth Registers, both as infants and as first time mothers between 1967-2009 (Norway) and 1973-2010 (Sweden). Risk of chronic hypertension in early pregnancy was calculated in women with perinatal exposures to preeclampsia, born SGA or preterm by log-binominal regression analysis, and adjusted for maternal age and level of education in the first generation. The rate of chronic hypertension was 0.4%. Risk of chronic hypertension was associated with single perinatal exposure to preeclampsia, being born SGA or preterm with adjusted relative risk (95% confidence interval, CI) of 2.2 (95% CI 1.8, 2.7), 1.1 (95% CI 1.0, 1.3), and 1.3 (95% CI 1.0, 1.5) respectively. The risks increased after joint exposures, with an almost fourfold risk increase after perinatal exposure to preeclampsia and preterm birth. Additional adjustment for BMI and smoking in the second generation in a subset of the cohort only had a minor impact on the results. Perinatal exposure to preeclampsia, being born SGA or preterm is independently associated with increased risk of chronic hypertension. The highest risk was seen after exposure to preeclampsia, especially if combined with SGA or preterm birth.

Foetal programming in the pathogenesis of arterial hypertension

Pathogenesis of arterial hypertension is complex and in spite of the decades of studies is not yet entirely understood. In recent years, attention has been paid to the phenomenon of foetal programming and its relationship to arterial hypertension in adult life. It has been shown that low birth weight predisposes to the development of arterial hypertension. The relationship between the number of nephrons and blood pressure and the risk of hypertension also has been found. Blood pressure and the number of nephrons depend on both genetic and environmental factors affecting pregnant females. The aim of this review is to summarize the current knowledge concerning the role of foetal programming in the pathogenesis of arterial hypertension in adults.

Pregnancy as a critical window for blood pressure regulation in mother and child: programming and reprogramming.

Pregnancy is a critical time for long-term blood pressure regulation in both mother and child. Pregnancies complicated by placental insufficiency, resulting in pre-eclampsia and intrauterine growth restriction, are associated with a threefold increased risk of the mother to develop hypertension later in life. In addition, these complications create an adverse intrauterine environment, which programmes the foetus and the second generation to develop hypertension in adult life. Female offspring born to a pregnancy complicated by placental insufficiency are at risk for pregnancy complications during their own pregnancies as well, resulting in a vicious circle with programmed risk for hypertension passing from generation to generation. Here, we review the epidemiology and mechanisms leading to the altered programming of blood pressure trajectories after pregnancies complicated by placental insufficiency. Although the underlying mechanisms leading to hypertension remain the subject of investigation, several abnormalities in angiotensin sensitivity, sodium handling, sympathetic activity, endothelial function and metabolic pathways are found in the mother after exposure to placental insufficiency. In the child, epigenetic modifications and disrupted organ development play a crucial role in programming of hypertension. We emphasize that pregnancy can be viewed as a window of opportunity to improve long-term cardiovascular health of both mother and child, and outline potential gains expected of improved preconceptional, perinatal and post-natal care to reduce the development of hypertension and the burden of cardiovascular disease later in life. Perinatal therapies aimed at reprogramming hypertension are a promising strategy to break the vicious circle of intergenerational programming of hypertension.

Invited Commentary: Hypertension and Arterial Stiffness--Origins Remain a Dilemma.

In this issue of the Journal, Chen et al. (Am J Epidemiol. 2016;183(7):599-608) present repeated measures of aorto-femoral pulse wave velocity, capacitive compliance (C1), and oscillatory compliance (C2) in the Bogalusa Heart Study, with the purpose of addressing which comes first: blood pressure elevation or arterial stiffening. After an average follow-up period of 7 years (2000-2010), the authors found that blood pressure at a mean age of 36 years predicted change in arterial stiffening by a mean age of 43 years, but not the reverse. Essential hypertension results from a mosaic of pathological mechanisms. It has been theorized that biological pathways involving increased sympathetic tone, insulin resistance, renin-angiotensin-aldosterone activation, and inflammation lead to hyperkinetic circulation, volume overload, and vascular remodeling. The resultant accelerated vascular aging may be assessed by determining the degree of arterial stiffness. The findings of Chen et al. add important empirical information to the literature but do not solve the dilemma regarding the origins of essential hypertension, partly because there are many techniques for estimating the many aspects of arterial stiffness which are not fully understood. Mathematical features of estimates might not be uniform across the age range. There is a need for tracking blood pressure and different aspects of arterial stiffness from childhood onward, with an aim of preventing hypertension in adult life.

Reprogramming: A Preventive Strategy in Hypertension Focusing on the Kidney.

Adulthood hypertension can be programmed in response to a suboptimal environment in early life. However, developmental plasticity also implies that one can prevent hypertension in adult life by administrating appropriate compounds during early development. We have termed this reprogramming. While the risk of hypertension has been assessed in many mother-child cohorts of human developmental programming, interventions necessary to prove causation and provide a reprogramming strategy are lacking. Since the developing kidney is particularly vulnerable to environmental insults and blood pressure is determined by kidney function, renal programming is considered key in developmental programming of hypertension. Common pathways, whereby both genetic and acquired developmental programming converge into the same phenotype, have been recognized. For instance, the same reprogramming interventions aimed at shifting nitric oxide (NO)-reactive oxygen species (ROS) balance, such as perinatal citrulline or melatonin supplements, can be protective in both genetic and developmentally programmed hypertension. Furthermore, a significantly increased expression of gene Ephx2 (soluble epoxide hydrolase) was noted in both genetic and acquired animal models of hypertension. Since a suboptimal environment is often multifactorial, such common reprogramming pathways are a practical finding for translation to the clinic. This review provides an overview of potential clinical applications of reprogramming strategies to prevent programmed hypertension. We emphasize the kidney in the following areas: mechanistic insights from human studies and animal models to interpret programmed hypertension; identified risk factors of human programmed hypertension from mother-child cohorts; and the impact of reprogramming strategies on programmed hypertension from animal models. It is critical that the observed effects on developmental reprogramming in animal models are replicated in human studies.

Antenatal betamethasone increases vascular reactivity to endothelin-1 by upregulation of CD38/cADPR signaling.

Antenatal steroid administration is associated with hypertension in adult life; however, the mechanisms underlying this phenomenon are unclear. The aim of this study was to further characterize the effects of antenatal glucocorticoid exposure on the endothelin (ET-1) system, specifically to ascertain the role of the cyclic adenosine diphosphate ribose (cADPR)/ryanodine receptor pathway in the increased sensitivity to ET-1 observed in the offspring exposed to antenatal glucocorticoids. Pregnant sheep were randomly treated with betamethasone (Beta; 0.17 mg/kg) or vehicle at 80 and 81 days of gestation. In adults, we studied endothelium-denuded arterial segments of the brachial arteries. ET-1-induced vasoconstriction was significantly higher in the arteries from Beta sheep (F=3.5, P<0.05). Inhibition of ADP-ribosyl cyclase with 2-2'-dihydroxy-azobenzene significantly decreased the ET-1-induced contraction in Beta but not in vehicle-treated sheep. Nicotinamide attenuated ET-1 contraction in both, but it was significantly more pronounced in the Beta-treated sheep. No significant differences were observed following KCl-induced (6.25-75 mM) contraction. Nicotinamide (10 mM) significantly attenuated the KCl-induced vasoconstriction in both groups. In KCl (62.5 mM)-constricted arteries, the effect of nicotinamide (NIC) was significantly greater in the vehicle-treated sheep (50% relaxation v. 40% relaxation; t=2.2, P<0.05). In contrast, the sodium nitroprusside (SNP) relaxation was not statistically different. An additive effect was observed when NIC and SNP were used in combination and it was also more pronounced in vehicle-treated sheep. We conclude that the increased response to ET-1 is mediated by activation of the CD38/cADPR signaling pathway. Further studies are required to identify the effectors downstream from cADPR affected by exposure to antenatal steroids.

CONSUMO DE SAL DE ADIÇÃO EM ALUNOS DO ENSINO MÉDIO ANTES E APÓS CONSCIENTIZAÇÃO SOBRE O CONSUMO DE SÓDIO

High blood pressure (HBP) is a multifactorial clinical condition characterized by high and sustained levels of blood pressure (BP), and the presence of elevated BP in childhood is predictor of hypertension in adult life. Studies have shown a positive correlation between sodium chloride ingested in the diet and blood pressure values. This study aims to evaluate the consumption of added salt before and after awareness of risk, by high school students. This occurred for three days in the refectory, where students received illustrative brochure with information about sodium intake; exhibition of a poster illustrating foods with their respective equivalent amount of sodium and sodium chloride, exemplifying the maximum recommended amount of consumption per day. For five days, before and after gaining awareness, it the amount of consumption of sachets of salt was accounted. Statistical analyzes were performed by Student's Test, with a confidence interval of 95%. During the study period were served on average 128.3 meals. Before the awareness of sodium consumption of risks, of 820mg and 330mg sodium salt was consumed an average per individual, and thereafter, 640mg and 260mg, respectively (p=0,043). Simple Nutrition Education Strategies in short term were effective for improving the consumption of added salt in adolescents.

The relation between birth weight and hypertension. A study among Danish nurses

The fetal origin hypothesis suggests that birth weight is related to several adult diseases. One hypothesis is that low birth weight is associated with increased risk of hypertension. ADDIN RW.CITE{{119 Barker,D.J. 2009}}In the present study we analyzed the association between self-reported birth weight and risk of hypertension with detailed confounder control, and the modification on this association by familial obesity and own weight history during childhood and youth. Methods: In 1999 the Danish Nurse Cohort study included 31,642 females aged 44 years or more of whom 76% replied to questions on birth weight, weight history, familial obesity disposition, parents socioeconomic status and presence of hypertension. Results: In total 14% reported birth weights below 3000 g. The univariate hazard ratio of hypertension for those born with birth weight 3000 g. The association remained stable after adjustment for important confounders, as lifestyle, weight history and socioeconomic status during upbringing. Conclusion: Our results support the hypothesis that low birth weight is associated with hypertension in adult life, also after considering several confounding factors and weight history later in life. Furthermore, the previous weight history might have an influence on the association between birth weight and the risk for adult hypertension.