Primary Cause Of Hypertension Research Articles

Primary Role of the Kidney in Pathogenesis of Hypertension.

Previous transplantation studies and the concept of 'nephron underdosing' support the idea that the kidney plays a crucial role in the development of essential hypertension. This suggests that there are genetic factors in the kidney that can either elevate or decrease blood pressure. The kidney normally maintains arterial pressure within a narrow range by employing the mechanism of pressure-natriuresis. Hypertension is induced when the pressure-natriuresis mechanism fails due to both subtle and overt kidney abnormalities. The inheritance of hypertension is believed to be polygenic, and essential hypertension may result from a combination of genetic variants that code for renal tubular sodium transporters or proteins involved in regulatory pathways. The renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS) are the major regulators of renal sodium reabsorption. Hyperactivity of either the RAAS or SNS leads to a rightward shift in the pressure-natriuresis curve. In other words, hypertension is induced when the activity of RAAS and SNS is not suppressed despite increased salt intake. Sodium overload, caused by increased intake and/or reduced renal excretion, not only leads to an expansion of plasma volume but also to an increase in systemic vascular resistance. Endothelial dysfunction is caused by an increased intracellular Na+ concentration, which inhibits endothelial nitric oxide (NO) synthase and reduces NO production. The stiffness of vascular smooth muscle cells is increased by the accumulation of intracellular Na+ and subsequent elevation of cytoplasmic Ca++ concentration. In contrast to the hemodynamic effects of osmotically active Na+, osmotically inactive Na+ stimulates immune cells and produces proinflammatory cytokines, which contribute to hypertension. When this occurs in the gut, the microbiota may become imbalanced, leading to intestinal inflammation and systemic hypertension. In conclusion, the primary cause of hypertension is sodium overload resulting from kidney dysregulation.

Sugar, salt, immunity and the cause of primary hypertension.

Despite its discovery more than 150 years ago, the cause of primary hypertension remains unknown. Most studies suggest that hypertension involves genetic, congenital or acquired risk factors that result in a relative inability of the kidney to excrete salt (sodium chloride) in the kidneys. Here we review recent studies that suggest there may be two phases, with an initial phase driven by renal vasoconstriction that causes low-grade ischemia to the kidney, followed by the infiltration of immune cells that leads to a local autoimmune reaction that maintains the renal vasoconstriction. Evidence suggests that multiple mechanisms could trigger the initial renal vasoconstriction, but one way may involve fructose that is provided in the diet (such as from table sugar or high fructose corn syrup) or produced endogenously. The fructose metabolism increases intracellular uric acid, which recruits NADPH oxidase to the mitochondria while inhibiting AMP-activated protein kinase. A drop in intracellular ATP level occurs, triggering a survival response. Leptin levels rise, triggering activation of the sympathetic central nervous system, while vasopressin levels rise, causing vasoconstriction in its own right and stimulating aldosterone production via the vasopressin 1b receptor. Low-grade renal injury and autoimmune-mediated inflammation occur. High-salt diets can amplify this process by raising osmolality and triggering more fructose production. Thus, primary hypertension may result from the overactivation of a survival response triggered by fructose metabolism. Restricting salt and sugar and hydrating with ample water may be helpful in the prevention of primary hypertension.

Hubungan antara peran keluarga dengan tingkat depresi pada lansia umur 45-59 tahun di posyandu lansia puskesmas dinoyo kecamatan lowokwaru kota malang

Hypertension is the beginning of various diseases that claimed the lives of so many people. Malignant disease commonly called the nickname "silent killer" which makes the patient trapped in the perception that he was in good health - just fine. High sodium intake is one of the main causes of primary hypertension, and family support is an alternative way of preventing sodium intake. This study aims to determine the relationship between family support for intake of sodium primary hypertension patients aged 45-59 years old. The research design used is descriptive correlative through cross sectional approach with the number of samples as many as 30 people in Puskesmas Dinoyo with sampling technique in total sampling. The data of the research were analyzed using spearman correlation and got the result of the respondents with the support of the family was in the category of less equal to 63,3% and sodium intake was in high category equal to 53,3%, result of analysis with correlation coefficient value equal to -0,534 with significance value equal to 0,002 which means the value of p <0.01 and Ha accepted that indicates a relationship between family support for sodium intake of hypertensive patients aged 45-59 years old at Puskesmas Dinoyo. The value of correlation coefficient of -0.534 which means the nature of the relationship is inversely proportional, the better the family support the lower the sodium intake. It is hoped that family members will give their maximum support to family members suffering from primary hypertension in terms of sodium intake.

Conocimientos de la hipertensión: Health beliefs about hypertension in an under-resourced community in the Dominican Republic.

Understanding health beliefs is important to facilitate health promotion and disease prevention as they influence health behaviors, outcomes, and disease management. Given the rise of hypertension-related diseases in the Dominican Republic, the purpose of our study was to identify hypertension-related health beliefs of Dominicans in order to inform the development of culturally appropriate interventions for hypertension prevention, care, and treatment. Semi-structured interviews were conducted with 20 Dominicans, 15 of whom were receiving treatment for hypertension. Operating within the interpretative paradigmatic framework, we conducted thematic analyses of interview data to identify hypertension-related health beliefs and practices. Iterative data analysis revealed the following themes: 1) Negative emotions are a primary cause of hypertension, 2) Medication is the best treatment but adherence is challenging, 3) Systemic barriers impede treatment access, 4) Hypertension negatively impacts mental and physical well-being, and 5) Lifestyle changes, relaxation, and social support help manage hypertension. Data gathered from member checking validated these findings. This study enhances understanding of the beliefs and experiences of Dominicans and emphasize the importance of implementing culturally competent health programming and care.

Hemodynamic Characterization of Primary Hypertension in Children and Adolescents.

BackgroundPrimary hypertension in children is often characterized by high pulse pressure that could be attributable to increased ventricular ejection velocities and volumes and/or increased arterial stiffness. The objective of this study was to examine the contributions of cardiac (ventricular ejection) and vascular (systemic vascular resistance, arterial stiffness, and pressure wave reflection) properties to primary hypertension in children and adolescents.Methods and ResultsChildren aged 8 to 18 years referred to a tertiary center for evaluation of hypertension and found to have primary hypertension (n=31) were compared with normotensive controls of similar age (n=50). Peripheral (brachial) and central (carotid) blood pressure waveforms and carotid‐femoral pulse wave velocity were measured by tonometry. Left ventricular outflow tract velocities and ejection volumes were measured by echocardiography. Wave separation and wave intensity analysis were used to assess pressure wave propagation. Increased mean arterial pressure in hypertensive children (90±15 versus 76±10 mmHg in hypertensive versus normotensive children; means±SD; P<0.001) was explained by increased heart rate and cardiac output (5.3±2.0 versus 4.5±1.2 L/min adjusted for age and sex; P<0.05) rather than increased systemic vascular resistance (18.0±4.6 versus 19.3±7.3 mmHg/min/mL; P=0.374). A more‐marked increase in pulsatility (peripheral pulse pressure 66±21 versus 46±12 mmHg; P<0.001) was explained by increased proximal aortic stiffness (pulse wave velocity, 3.3±1.4 versus 2.5±0.8 m/s; P<0.005) and increased left ventricular ejection velocity (1.33±0.24 versus 1.21±0.18 m/s; P<0.05).ConclusionsCardiac overactivity characterized by increased heart rate and left ventricular ejection velocities and increased proximal pulse wave velocity may be the main cause of primary hypertension in children.

Hypertension in obesity.

The obesity epidemic is progressively affecting majority of individuals worldwide leading to many adverse metabolic and cardiovascular outcomes. Increasingly concerning among them is obesity hypertension (HTN). In this review, we delve into the physiology and therapeutic options in obesity HTN as we discuss the implications of obesity HTN on society. Obesity is the most common cause of primary HTN and is directly proportional to increases BMI. The significance of adiposity in obesity HTN centers on humoral mechanisms via stimulation of the renal-angiotensin system, leptin activity, sympathetic overdrive, and proinflammatory processes that potentiate vascular remodeling, which results in a higher incidence of the progression of many known serious cardiovascular diseases. Although lifestyle and medical therapies have been recommended for obesity and its sequelae, continued global progression of this disease has driven the development of newer therapies such as carotid baroreflex activation therapy, renal denervation, and selective leptin receptor antagonism. The pathophysiology of obesity HTN has not yet been fully elucidated despite it being one of the oldest known diseases to mankind. Major efforts to understand obesity HTN endures, paving opportunities for newer and possibly superior therapeutic options.

Plasma total calcium concentration is associated with blood pressure and systemic vascular resistance in normotensive and never-treated hypertensive subjects

Purpose: The underlying causes of primary hypertension are not fully understood. Evidence on the relation of plasma calcium concentration with blood pressure (BP) is inconsistent and relies largely on studies utilizing office BP measurements in populations using cardiovascular drugs. In many studies adjustment for confounders was not optimal. In this cross-sectional study we examined the association of plasma total calcium concentration with the haemodynamic determinants of blood pressure.Subjects and methods: Supine haemodynamics were recorded using pulse wave analysis, whole-body impedance cardiography, and heart rate variability analysis in 618 normotensive or never-treated hypertensive subjects (aged 19–72 years) without diabetes, cardiovascular or renal disease, or cardiovascular medications. Linear regression analysis was used to investigate factors associated with haemodynamic variables.Results: Mean age was 45.0 years, body mass index 26.8 kg/m2, seated office BP 141/89 mmHg, and 307 subjects (49.7%) were male. Mean values of routine blood and plasma chemistry analyses were within the reference limits of the tests except for low-density lipoprotein cholesterol (3.05 mmol/l). In the laboratory, mean supine radial BP was 131/75 mmHg, and both systolic and diastolic BP correlated directly with plasma total calcium concentration (r = 0.25 and r = 0.22, respectively, p < 0.001 for both). In regression analysis plasma total calcium concentration was an independent explanatory variable for radial and aortic systolic and diastolic BP, and systemic vascular resistance, but not for cardiac output, pulse wave velocity, or any of the heart rate variability parameters.Conclusion: Plasma total calcium concentration was directly associated with systolic and diastolic BP and systemic vascular resistance in normotensive or never-treated hypertensive subjects without comorbidities and cardiovascular medications. Higher plasma calcium concentration potentially plays a role in primary hypertension via an effect on vascular resistance.

Two Cases of Guillain-Barré Syndrome Variants Presenting With Dysautonomia.

We describe 2 pediatric cases presenting with posterior reversible encephalopathy syndrome secondary to autonomic dysfunction preceding the onset of motor symptoms in Guillain-Barré syndrome variants. Patient 1 presented acutely with encephalopathy, cerebellar signs, hypertension, lower limb weakness, and respiratory decompensation. Magnetic resonance imaging (MRI) brain showed occipital lesions consistent with posterior reversible encephalopathy syndrome. Nerve conduction studies were consistent with Miller-Fisher syndrome. After intravenous immunoglobulin and plasmapheresis, he improved clinically with radiological resolution. Patient 2 presented with headache, leg pain, seizures, and significant hypertension. Brain MRI was normal but spine MRI revealed enhancement of the cauda equina ventral nerve roots. She was areflexic with lower limb weakness a few days after intensive care unit admission and made a significant improvement after treatment with intravenous immunoglobulin. In children presenting with posterior reversible encephalopathy syndrome in the absent of other causes of primary hypertension, Guillain-Barré syndrome variants are an important differential etiology, presenting with autonomic dysfunction, even before signs of motor weakness become evident.

Protocol of randomized control trial for effectiveness of angiotensin receptor blockers on blood pressure control among euvolemic hypertensive hemodialysis patients.

Introduction:Volume overload and the renin–aldosterone–angiotensin system (RAAS) are 2 major factors contributing to hypertension (HTN) among hemodialysis (HD) patients. Although volume-dependent components of HTN can be corrected by appropriate volume removal, a proportion of HD patients experience elevated blood pressure (BP) despite achieving euvolemic and ideal dry weight.Method and analysis:A single center, prospective, randomized, parallel design, single-blind trial will be conducted in the Malaysian state of Kelantan among postdialysis euvolemic hypertensive patients that are on regular dialysis at least 3 times a week. The primary outcome of the trial will be to note the effectiveness of losartan (RAAS inhibitor) in reducing systolic BP < 140 mm Hg compared to standard non-RAAS-inhibitor antihypertensive therapy. The secondary outcome will be to look at all causes of mortality. A body composition monitor (BCM) will be used to assess postdialysis volume and dry weight. Postdialysis euvolemic patients that have systolic BP > 140 mm Hg will be randomized using Covariate Adaptive Randomization to standard or treatment arm. Participants in the treatment arm will be given 50 mg of losartan once daily except on dialysis days, whereas the standard arm patients will be prescribed non-RAAS antihypertensive agents. The study participants will be followed for a period of 12 months. A Wilcoxon statistical test will be performed to note the difference in BP from baseline up to 12 months using Statistical Package for the Social Sciences (SPSS) 20.Ethical and trial registration:The study protocols are approved from the Ethical and Research Committee of the Universiti Sains Malaysia (USM/JEPeM/15050173). The trial is registered under the Australia New Zealand Clinical Trial Registry (ACTRN12615001322527). The trial was registered on 2/12/2015 and the 1st patient was enrolled on 10/12/2015. The trial was formally initiated on 16/02/2016.Conclusion:Management of HTN among HD patients requires understanding the primary cause of HTN and treating accordingly. The current trial is an attempt to reduce BP among postdialysis euvolemic but hypertensive patients.

Regulation of Renal Hemodynamics and Function by RGS2.

Regulator of G protein signaling 2 (RGS2) controls G protein coupled receptor (GPCR) signaling by acting as a GTPase-activating protein for heterotrimeric G proteins. Certain Rgs2 gene mutations have been linked to human hypertension. Renal RGS2 deficiency is sufficient to cause hypertension in mice; however, the pathological mechanisms are unknown. Here we determined how the loss of RGS2 affects renal function. We examined renal hemodynamics and tubular function by monitoring renal blood flow (RBF), glomerular filtration rate (GFR), epithelial sodium channel (ENaC) expression and localization, and pressure natriuresis in wild type (WT) and RGS2 null (RGS2-/-) mice. Pressure natriuresis was determined by stepwise increases in renal perfusion pressure (RPP) and blood flow, or by systemic blockade of nitric oxide synthase with L-NG-Nitroarginine methyl ester (L-NAME). Baseline GFR was markedly decreased in RGS2-/- mice compared to WT controls (5.0 ± 0.8 vs. 2.5 ± 0.1 μl/min/g body weight, p<0.01). RBF was reduced (35.4 ± 3.6 vs. 29.1 ± 2.1 μl/min/g body weight, p=0.08) while renal vascular resistance (RVR; 2.1 ± 0.2 vs. 3.0 ± 0.2 mmHg/μl/min/g body weight, p<0.01) was elevated in RGS2-/- compared to WT mice. RGS2 deficiency caused decreased sensitivity and magnitude of changes in RVR and RBF after a step increase in RPP. The acute pressure–natriuresis curve was shifted rightward in RGS2-/- relative to WT mice. Sodium excretion rate following increased RPP by L-NAME was markedly decreased in RGS2-/- mice and accompanied by increased translocation of ENaC to the luminal wall. We conclude that RGS2 deficiency impairs renal function and autoregulation by increasing renal vascular resistance and reducing renal blood flow. These changes impair renal sodium handling by favoring sodium retention. The findings provide a new line of evidence for renal dysfunction as a primary cause of hypertension.

Zinc and Copper Levels in Patients with Primary Hypertension and Normotension

One of the causes of primary hypertension is an exposure to free radicals. The formation of free radicals in the body can be prevented by taking antioxidants. Zinc and copper are cofactors of endogenous antioxidant enzyme superoxide dismutase. This study aimed to analyze the differences of zinc and copper levels in primary hypertensive and normotensive patients. This was an analytical observational study with cross sectional design and simple random sampling method. Subjects were patients aged 40-70 years at Haji General Hospital consisting of 15 primary hypertensive patients and 15 normotensive individuals (comparison group). Data was collected through interviews and laboratory test of blood samples. Zinc and Copper serum concentrations were measured by AAS. Data were analyzed by chi-square and independent samples t-test. The results showed that the mean levels of zinc and copper in primary hypertensive patients was lower than normotensive. However, statistically there was no difference in zinc serum levels (p=0.852) in the two groups, and there was a significant difference in copper serum levels (p=0.032). It can be concluded that there were differences in copper serum levels between the two groups but not with the levels of zinc.

Treatment of Hypertension in Patients with Atherosclerotic Renal Artery Stenosis, Updated

Atherosclerotic renal artery stenosis (ARAS) is a fairly common disease of elderly patients and is discovered incidentally in 6.3% to 38% in those undergoing diagnostic cardiac or abdominal angiography. Of those patients diagnosed with renal artery stenosis, in 90% it is due to ARAS and in 10% to fibromuscular dysplasia (FMD), which is a disease of younger persons, mostly females. Renal artery stenosis is frequently associated with hypertension and impaired renal function, and it is perceived by many physicians as the primary cause of hypertension and renal failure. For this reason, they believe that hypertension and renal failure can be significantly improved by performing percutaneous transluminal renal angioplasty (PTRA) with a stent placement as the preferred treatment instead of medical therapy. This practice has led to an increase in angioplasties, especially by interventional cardiologists who are familiar with the procedure. However, the results of several randomized studies comparing interventional therapy with medical therapy have shown no significant difference between the 2 treatment modalities in blood pressure reduction and prevention and in worsening of renal function. Similar results have been found by nonrandomized trials in patients treated selectively with PTRA. For this review, a Medline search was conducted of the English-language literature from January 1, 2006 to December 31, 2013, using the terms atherosclerotic renal artery stenosis and renal artery stenosis; 6 pertinent randomized studies were selected. These studies, with collateral literature, are discussed in this review. The data show that PTRA with stent plus medical therapy in patients with ARAS is not superior to medical therapy alone in lowering the blood pressure, in preventing renal function deterioration, and in reducing all-cause mortality, cardiovascular morbidity or mortality, and strokes.

Abstract 640: RGS2 Deficiency Impairs Renal Hemodynamics and Function

Regulator of G protein signaling 2 (RGS2) regulates signaling by acting as a GTPase-activating protein for Gq/11α and Gi/oα subunits of heterotrimeric G proteins. Certain single nucleotide polymorphisms and loss-of-function mutations of RGS2 have been linked to human hypertension. RGS2 deficiency in the kidney is sufficient to cause hypertension in mice; however, the renal pathophysiological mechanisms are unknown. Here, we assessed renal hemodynamics and function using renal blood flow (RBF) and glomerular filtration rate (GFR) measurements, and assessment of pressure natriuresis in wild type (WT) and RGS2 null (RGS2-/-) mice. GFR was measured by plasma clearance of FITC-inulin. Pressure natriuresis was determined by increasing renal perfusion pressure (RPP) stepwise by clamping the superior mesenteric and celiac arteries, and abdominal aorta, while total RBF was simultaneously recorded with flow probe. Baseline GFR was markedly decreased in RGS2-/- mice compared to WT controls (1.8 ± 0.1 vs. 1.1 ± 0.1 ml/min/g kidney weight, p=0.004). Renal conductance was reduced (70 ± 9 vs. 51 ± 3 μl/min/g kidney weight, p=0.006) while renal vascular resistance (RVR; 14.9 ± 2.2 vs. 20.2 ± 1.3 mmHg/ml/min/g kidney weight, p=0.002) was elevated in RGS2-/- compared to WT mice. The absence of RGS2 resulted in decreased sensitivity and magnitude of change in RVR (WT: 11.17 ± 1.94 vs. RGS2-/-: 6.87 ± 0.90 mmHg/ml/min/g) and conductance (WT: -25.69 ± 3.22 vs. RGS2-/-: -13.87 ± 2.40 ml/min/mmHg/g) after a step increase in RPP. The acute pressure-natriuresis curve shifted rightward in RGS2-/- relative to WT, with no change in the slope. Fractional sodium excretion was unaffected by RGS2 deficiency. We conclude that RGS2 deficiency impairs renal function and autoregulation by increasing renal vascular resistance and reducing effective renal blood flow. The findings provide a new line of evidence for renal vascular dysfunction as a primary cause of hypertension. Mutations or downregulation of RGS2 in the kidney may contribute to human hypertension by causing renal hypoperfusion and decreased GFR. Signaling pathways regulated by RGS2 may provide therapeutic targets in hypertension patients harboring mutations that potentially decrease expression and/or function of RGS2.

Medication adherence in a sample of elderly suffering from hypertension: evaluating the influence of illness perceptions, treatment beliefs, and illness burden.

Although many advances in the management of hypertension have been made, success in hypertension control in real-life practice is limited. Control of hypertension is paramount in primary as well as secondary prevention of cardiovascular disease. Poor adherence to antihypertensive medication is one possible reason why success in clinical trials has not been translated into everyday practice. Despite many years of study, questions remain about why patients do or do not take medicines and what can be done to change their behavior. Although trends in adherence patterns across hypertensive patients is briefly documented in the literature, the role of perceived illness burden in addition to illness perceptions and medication beliefs in elderly people with hypertension is unclear. To assess the collective influence of illness perceptions, medications beliefs, and illness burden on medication adherence of a sample of elderly people suffering from hypertension. A cross-sectional questionnaire survey research design, utilizing convenience sampling strategies and a battery of self-administered health surveys, was adapted to address key study objectives. Previously validated instruments, such as the Brief Illness Perception Questionnaire, Pictorial Representation of Illness and Self Measure Revised II, Beliefs about Medicines Questionnaire, and Morisky Medication Adherence Scale, were utilized to assess illness perceptions, perceived illness burden, medication beliefs, and medication adherence, respectively. Conceptualized associations among the study variables were explored and tested to assess their individual, as well as collective, impact on medication adherence. In addition, combined predictive abilities of key variables in explaining the variations in medication adherence were determined using appropriate bivariate and multivariate statistics. The majority of the sample was white (76.9%); 52.1% was over aged 65 years of which 47.9% attended some college, while 70.1% accessed adult day care centers. A usable sample of 117 respondents was retained for statistical analysis. From multiple linear regression analysis, it was observed that perceptions about illness, perceived illness burden, and beliefs about medication jointly played a significant role in the prediction of medication adherence (R-squared = 0.328). Significant bivariate correlations among study variables further indicated that threatening view of illness translated into higher levels of self-reported adherence with hypertensive medications (r = 0.332, P < 0.001), which in turn was associated with lower perceived illness burden (r = 0.423, -0.444, P < 0.001). The respondents reported illness-related “Stress” (49.1%) as a primary cause of hypertension in their opinion, followed by “Lifestyle” (43.8%) and “Heredity” (7.1%) factors. Perceived concerns about the benefits of medication played a more significant role in the prediction of adherence and perceived illness burden than the risks associated with their use. This study provides insights into how perceptions of illness and burden relate to medication adherence in hypertension. More benign perceptions of illness and greater perceived illness burden translate to lower medication adherence. Positive beliefs regarding medications are also crucial for shaping adherence behavior of elderly hypertensive individuals. Threatening views of illness and stronger beliefs of the necessity of medications contribute substantially to positive medication adherence. Interventions and programs aimed at building adherence in elderly hypertension patients need to recognize the value and importance of patient perceptions of illness and medications in shaping adherence behavior.

OBESITY AND ANGIOTENSIN II

Pathogenesis of hypertension in overweight and obese patients is to be studied due to the great theoretical and practical importance. The additional mechanisms directly involved in the development of hypertension in subjects with abdominal obesity have been determined. Functional disorders of adipose tissue were shown to play an important role in the development of hypertension in obese patients, and in some cases adiposopathy can be the primary cause of hypertension. Renin-angiotensin-aldosterone system was shown to change signifi cantly in obesity. Understanding the causes and mechanisms of hypertension in patients with abdominal obesity is of particular interest because it allows more focused prevention and treatment of the disease.

Implications of Salt and Sodium Reduction on Microbial Food Safety

Excess sodium consumption has been cited as a primary cause of hypertension and cardiovascular diseases. Salt (sodium chloride) is considered the main source of sodium in the human diet, and it is estimated that processed foods and restaurant foods contribute 80% of the daily intake of sodium in most of the Western world. However, ample research demonstrates the efficacy of sodium chloride against pathogenic and spoilage microorganisms in a variety of food systems. Notable examples of the utility and necessity of sodium chloride include the inhibition of growth and toxin production by Clostridium botulinum in processed meats and cheeses. Other sodium salts contributing to the overall sodium consumption are also very important in the prevention of spoilage and/or growth of microorganisms in foods. For example, sodium lactate and sodium diacetate are widely used in conjunction with sodium chloride to prevent the growth of Listeria monocytogenes and lactic acid bacteria in ready-to-eat meats. These and other examples underscore the necessity of sodium salts, particularly sodium chloride, for the production of safe, wholesome foods. Key literature on the antimicrobial properties of sodium chloride in foods is reviewed here to address the impact of salt and sodium reduction or replacement on microbiological food safety and quality.

Prenatal programming and the development of hypertension

The kidney has a predominant role in fluid and electrolyte homeostasis and the nephron is the functional. Disturbances in its function may result in hypertension due to volume overload and/or activation of the renin angiotensin aldosterone system. Thus, it is not surprising that diseases of the kidney or its vasculature are the leading causes of secondary hypertension. Moreover, in recent years, reductions of nephron number have been implicated as a cause of primary hypertension. Barker was the first to describe the role of prenatal factors in the development of hypertension, though the morphological correlate was unclear until very recently. A large Finish study in humans has shown that the birth weight is inversely correlated with the development of hypertension later in life. Similar results were presented this year by a Dutch group studying the effects of the “hunger winter“ in Arnhem. Potential mechanisms include the upregulation of specified sodium transporters and increased activity of components of the renin angiotensin aldosterone system as well as the sympathetic nervous system. Studies in rats and sheep have now demonstrated that prenatal exposure to dexamethasone as well as various dietary restrictions to mother animals may result in hypertension of the respective offspring. These changes in blood pressure were accompanied by reductions in nephron number. It is unclear if these changes apply to humans as well. Our own studies examine the changes induced by prenatal dexamethasone exposure in marmoset monkeys as part of the EUPEAH project. First result will be presented at the meeting and the findings will be discussed in the context of the current literature.

The Effect of Therapeutic Back Massage in Hypertensive Persons: A Preliminary Study

Hypertension, one of the most pervasive disease processes in the United States, can lead to target organ damage. Although there is no one cause of primary hypertension, the theory of an unchecked long-term stress response continues to be a valid argument. Conversely, eliciting the relaxation response may alter the course of the unchecked stress response. Massage therapists have suggested that their therapy elicits the relaxation response and therefore can decrease blood pressure (BP) and hypertension. This preliminary study tested the effects of a regularly applied back massage on the BP of patients with clinically diagnosed hypertension. In this experimental, pretest-posttest study, a 10-min back massage was given to the experimental group (n = 8), three times a week for 10 sessions. The control group (n = 6) relaxed in the same environment for 10 min, three times a week for 10 sessions. Analysis of variance determined systolic BP changed significantly, F(1, 12) = 17.90, p = .001, between groups over time as did the diastolic BP, F(1, 12) = 8.34, p = .014. Effect size was 2.25 for systolic pressure and 1.56 for diastolic pressure (alpha of .05 and power at .80). This preliminary study suggests that regular massage may lower BP in hypertensive persons.

Interactions between the sympathetic nervous system and the kidneys in arterial hypertension.

Elevated sympathetic activity changes renal function and accelerates the development of hypertension. Principles of sympatho-renal interactions in chronic hypertension are reviewed. Alterations in the ontogeny of the sympathetic nervous system and the kidney, inherited abnormalities in sensory receptor function and exaggerated responsiveness to mental stress contribute to inappropriately high sympathetic activity in primary or essential hypertension. Careful characterization of clinical study populations shows that elevated sympathetic activity and "essential" hypertension are not unequivocally associated. Prospective clinical studies which investigate a broader array of physiological functions and experiments in recombinant inbred rodents with less traumatic nerve recording techniques than currently available will help to define under which conditions elevated sympathetic activity is indeed a cause of primary hypertension. Signals arising from the kidney which activate the renin-angiotensin system and afferent renal nerves increase sympathetic activity. These mechanisms importantly contribute to the pathogenesis of hypertension secondary to renal artery stenosis and end-stage renal disease.

Pathogenesis and clinical physiology of hypertension

Although the definitive cause of primary hypertension remains unknown, its pathogenesis and clinical history are relatively well understood. Genes, environment, and their interaction play crucial roles in the development of hypertension. Elevated blood pressure levels are maintained through alterations in multiple BP regulatory systems including the central and peripheral nervous system, renin-angiotensin-aldosterone system, renal mechanisms, structural and functional changes in the vascular wall and endothelium, and multiple feedback loops involving a wide spectrum of receptors and.