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This chapter describes an interdisciplinary research program that studied individual and group differences in the risk for hypertension and heart disease. The differences studied include ones relating to: gender and racial group; family history of hypertension; personality and psychosocial traits like hostility, pessimism, and low social resources; and high versus low cardiovascular and renal responders to lab stressors. Among the findings is that potential behavioral risk factors should be studied in combination with markers of genetic risk for hypertension. The chapter also discusses the factors that encouraged this interdisciplinary research (including access to medical school colleagues and resources and NIH support) and the factors that impeded this work.

Success in diagnosing and treating age-related brain disease depends on understanding normative and optimal aging of the brain. Neuroimaging studies of healthy adults reveal differential brain shrinkage. Prefrontal cortices evidence the largest age-related differences, whereas tertiary association cortices, the neostriatum, and the cerebellum show the greatest rate of shrinkage. Reduced regional brain volumes and steeper longitudinal declines are usually associated with lower cognitive performance. Trajectories of differential brain aging are modified by multiple negative and positive factors. Vascular risk factors affect the regions deemed most vulnerable to aging. However, the positive modifying influence of aerobic fitness is clearest in the same age-sensitive areas. Genetic variation may have a significant impact on age-related changes in brain and cognition. In addition to (and in conjunction with) improved aerobic fitness, antihypertensive treatment and hormone replacement therapy may alleviate negative effects of aging on the brain structure.

Franklin, an African American firefighter, sustained third-degree burns on his left arm and hand when he attempted to free a child from a burning vehicle without success. Months following this incident, Franklin was diagnosed with hypertension and his physician prescribed an antihypertensive medication to lower it. However, Franklin took the medication only if he encountered a particularly stressful period on the job or at home. Like Franklin, millions of people worldwide do not really have a comprehensive understanding of their diagnosis of hypertension. Most people believe that stress is the reason their blood pressure is high, so they choose to discontinue treatment during less stressful periods. This book aims to provide an understanding of hypertension and its complex relationship with stress. It examines the body of empirical evidence testing the assumption that stress is associated with the onset and maintenance of essential hypertension.

This chapter summarizes the wealth of recent evidence to support the epidemiological link between quantity of sleep (short and long duration of sleep) and quality of sleep (like difficulties in falling asleep or of maintaining sleep), and both fatal and non-fatal cardiovascular outcomes, like myocardial infarction (MI) and stroke, and cardiovascular risk factors, namely hypertension, obesity, type 2 diabetes and other disturbances of glucose metabolism, and lipids. It describes observed gender differences in the risk and the meaning of U-shaped relationships, which in part may reflect different pathways and potential mechanisms. As the potential population and public health implications of such findings may be significant, it is imperative that the causality of the associations described be determined and the reversibility of the effects tested.

Sleep has a significant impact on breathing through withdrawal of the wakefulness stimulus and alterations in muscle tone, ventilatory chemosensitivity, lung properties, and metabolic rate. Obstructive sleep apnea and sleep-related hypoventilation are highly prevalent and frequently unrecognized sleep breathing disorders, which have a significant impact on health. Among the many factors promoting their development, obesity represents the most important modifiable risk factor. There is increased recognition that a dual interaction between sleep/sleep disorders and chronic lung disease exists. On the one hand, there is increased prevalence of globally disturbed sleep, insomnia, and restless legs syndrome in chronic lung disease. On the other hand, sleep is a vulnerable time for these patients and there is data to suggest worse respiratory outcomes and quality of life in patients with coexistenting sleep disorders. Many gaps remain in our knowledge of the nature of these interactions, their underlying mechanisms, and implications for these already compromised populations.

The aetiology of hypertension remains obscure in the majority of cases, and treatment, therefore, somewhat empirical. However, abnormalities in the structure and function of the vasculature are increasingly recognized as contributing to the hypertensive state by increasing total peripheral resistance. This chapter briefly reviews some of these abnormalities with particular regard to the way in which they influence treatment, and suggests new therapeutic strategies. A minority of hypertensive individuals have a clearly identified hormonal or structural cause for their elevated pressure (‘secondary hypertension’) and are not specifically considered further here, although some animal models rely on such aetiologies to produce hypertension for experimental purposes.

Indirect causes of childhood obesity are complex and are sometimes linked to psychological factors, social expectation or pressure, and fat stigmatization. Obesity in children may also be somewhat attributed to psychological stress such as low esteem, poor peer acceptance, and low participation in social and sport activities. However, in some African cultures, particularly those living in rural areas and a minority in urban areas who still follow indigenous knowledge, obesity in both children and adults is regarded as a sign of wealth, status, and physical attractiveness. This chapter reviews child and youth obesity (aged between 1 and 24 years) and hypertension trends and prevention strategies in South Africa, using individual studies conducted in both rural and urban settings and the national studies during the 21st century.

Intracellular signaling activities in vascular smooth muscles (VSMs) are central in the control of blood vessel diameter and the regulation of peripheral vascular resistance and blood pressure. Several studies have examined the molecular mechanisms underlying VSM contraction under physiological conditions and the pathological alterations that occur in vascular diseases such as hypertension. Vasoconstrictor stimuli activate specific cell surface receptors and cause an increase in intracellular free Ca²⁺ concentration ([Ca²⁺]_i), which forms a complex with calmodulin, activates myosin light chain (MLC) kinase, and leads to MLC phosphorylation, actin-myosin interaction, and VSM contraction. In unison, activation of protein kinase C (PKC) increases the myofilament force sensitivity to [Ca²⁺]_i and MLC phosphorylation, and maintains VSM contraction. Identifying the subcellular location of PKC may be useful in the diagnosis and prognosis of VSM hyperactivity states associated with hypertension. Targeting of vascular PKC using isoform-specific PKC inhibitors may work in concert with cytokine antagonists, antioxidants, and matrix metalloproteinase inhibitors, and thereby provide new approaches in the treatment of VSM hyperactivity states and certain forms of hypertension that do not respond to Ca²⁺-channel blockers.

This chapter presents a case for a patient with an overactive adrenal gland. The adrenal gland can be the site of hormonally active or inactive lesions, benign or malignant tumors, metastases, and infections. The prognosis in patients having an adrenal abnormality depends not only on the benign or malignant character of the lesion but also on its hormonal activity. For example, patients with primary aldosteronism can suffer from resistant hypertension with its chronic complications, patients with phaeochromocytoma can present in a hypertensive crisis that can be fatal and patients with Cushing's syndrome have high risks of atherosclerosis, thrombosis, and osteoporosis. These situations can often be prevented or reversed by an accurate assessment including careful evaluation of clinical, biochemical, and morphological features. Matching the optimal therapy with the cause can usually often produce a definitive solution.

The hypothalamus plays a key role in regulating autonomic function, usually as part of more generalized, often quite stereotyped, behavioural responses triggered by internal challenges (e.g., a change in body temperature or blood glucose levels) or external threats (e.g., the sight, sound or odour of a predator). Neurons within hypothalamic nuclei (especially the paraventricular nucleus, dorsomedial hypothalamus and perifornical area) make direct and indirect connections with sympathetic and parasympathetic preganglionic neurons and, in turn, receive inputs from a wide variety of sources, including (1) visceral and pain receptors, (2) receptors in circumventricular organs signalling changes in blood levels of circulating substances, and (3) inputs from the external environment, such as inputs signalling changes in temperature, light, and odour. Hypothalamic nuclei, especially the paraventricular nucleus and dorsomedial hypothalamus, are believed to generate the marked increases in sympathetic activity associated with disorders, such as neurogenic hypertension, severe heart failure and panic disorder.

The ventrolateral medulla plays a critical role in the regulation of arterial blood pressure, mainly by regulating sympathetic nerve activity to cardiovascular targets such as the heart and blood vessels. This chapter focuses on the rat as an experimental model and discusses how different regions of the ventrolateral medulla, which are organized into semi-continuous columns, maintain basal sympathetic nerve activity to vascular targets in health and in diseases such as hypertension. The chapter emphasizes the importance of sympathoexcitatory neurons in the rostral ventrolateral medulla, and neurons in the caudal ventrolateral medulla that inhibit them, in the short term regulation of arterial pressure through effects on sympathetic reflexes. The chapter summarizes the extensive body of anatomical and physiological information about these neurons and highlights the on-going pursuit to better understand how these critical neurons are regulated in normotensive and hypertensive states.

Early-life events influence late life health. An adverse early environment changes the developing organism's metabolism, physiology, and organ structure to increase risk of adult metabolic disorders, including the metabolic syndrome, diabetes, and cardiovascular disease. Early environmental cues initiate functionally coherent adjustments that alter energy-partitioning and modify nutritional requirements. When maternal nutritional and endocrine cues predict future environmental conditions, developmental and metabolic responses to these cues could provide a mechanism for fine-tuning responses to local environmental conditions. However, individuals faced with scarcity early in life are now increasingly confronted with abundance later in life, and the resulting mismatch between the environment early and late in life is an important contributor to patterns of human morbidity and mortality.

We evolved under high levels of physical activity and energy expenditure, seasonal fluctuations in food availability, and frequent periods of marginal or negative energy balance. Today, we continue to eat about the same amount but exercise less, and the ‘imbalance’ between energy intake and expenditure causes obesity. Consumption of meat from feedlot animals now causes atherosclerosis; eating wild or grass-fed animals does not. For most of human history, simple carbohydrates were a minor element of our diet; today Americans derive almost 40% of calories from simple sugars and refined grain products. Simple carbohydrates contribute to the rise of type 2 diabetes in the industrialized world. The problems of ‘overnutrition’ and energy surplus are causing rates of obesity, diabetes, and hypertension to increase more rapidly in the developing than in the industrialized world. Nutritional interventions should promote increased exercise and activity levels as well as dietary modifications.

High blood pressure, commonly referred to as hypertension, takes two forms: primary or essential hypertension and secondary hypertension. In cases of secondary hypertension, there is an identified physiological abnormality or exogenous substances causing the high blood pressure. When the exact cause of the elevated blood pressure is unknown, the condition is called primary or essential hypertension. This chapter examines studies that present evidence linking stress with the onset of essential hypertension. These studies are categorized into several different types: studies of major life event stressors, studies of job stress and strain, studies on cultural influences on stress and blood pressure, and animal research linking stress to hypertension.

This chapter examines colour vision in patients with an early stage of arterial hypertension without end-organ damage. A significantly higher median error score in Roth's 28-hue (E) desaturated colour-arrangement test was observed for patients with arterial hypertension than for the control group. These results should be taken into account in colour-vision testing to avoid diagnostic interference between specifically ocular diseases (e.g. glaucoma) and arterial hypertension.

This chapter traces the intellectual roots of cost-effectiveness analysis in health care. It also provides a brief history of CEA in health applications. It argues that the emergence of CEA in the 1960s and 1970s represented a paradigm shift in that it reflected a growing awareness that American medicine had exceeded society's capacity to pay for all of the health care that people could use to actually improve their health. It highlights that in 1970s and early 1980s, cost-effectiveness analyses of health problems began to appear in major medical journals, including influential papers examining the cost-effectiveness of inexpensive tests for cancer screening, of strategies to manage hypertension, and of vaccines for pneumococcal pneumonia.

Heart disease has been the leading cause of death in the United States since 1921, and stroke has been the third leading cause since 1938. Heart disease and stroke account for most cardiovascular disease (CVD) deaths in the United States. Although heart disease and stroke remain leading causes of death, age-adjusted death rates from all CVD have declined by 55% since 1950. This decline reflects an increased understanding of the causes of CVD, identification of preventable risk factors, improvements in treatment of heart disease and stroke and their antecedents such as hypertension, and implementation of intervention and prevention programs. This chapter summarizes the trends in heart disease and stroke in the 20th century, advances in the understanding of risk factors for these diseases, and development of prevention and intervention programs to reduce the risks of developing and dying from heart disease and stroke.

Reproductive events throughout a woman's life course tend to be both a product of the cumulative exposures a woman has been subject to before that event, as well as a marker for her likely future health. While genetic contributions influence the fertility, development, growth, and reproduction of the next generation, all of these critical events in life are subject to external, environmental influences. This is true for individual women and within families of individuals. Perhaps given the shared genes and environments within and across generations in a family it is therefore not surprising that family studies consistently demonstrate a higher degree of consistency in reproductive outcomes at all points in the life course for those who share a family connection, than for individuals who do not, and that the closer that connection (e.g., monozygotic twins) in general the greater the similarities.

We live in an environment that differs in many important respects from the environments in which our ancestors lived and to which they became more or less well adapted. We live in large, culturally diverse, and socioeconomically stratified communities of genetically unrelated individuals; we eat different foods; we are exposed to different sets of pathogens and toxins; and we have different patterns of physical activity than did our ancestors. These culturally constructed or man-made environmental changes have resulted in an epidemiologic transition. As deaths from famine and infectious diseases decreased, and life expectancy increased, the burden of disease has shifted to chronic, noncommunicable diseases such as diabetes, coronary heart disease, and stroke. These diseases, which are often referred to as Western diseases, are more appropriately thought of as man-made diseases. Changes in diet, particularly increases in the consumption of sucrose, high fructose corn syrup, and salt, have led to increases in obesity, diabetes, and hypertension. Reducing the prevalence of these diseases requires interventions that reduce risk factors in the entire population. According to the hygiene hypothesis, reduction in exposure to helminths and other pathogens has resulted in an increased risk of allergic and autoimmune diseases. This hypothesis has led to novel, helminth-based treatment of patients with these diseases. Finally, socioeconomic disparities in physiological capital and in psychosocial stresses have led to health disparities. Reducing socioeconomic disparities is the most promising approach to ameliorating health disparities.