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Given the prevalence and impact of hypertension on vascular disease in diabetic patients, the prevalence, awareness, treatment, and control of hypertension in diabetes has important implications for healthcare policy and professional guidelines. This report examines changes in the clinical epidemiology of hypertension in diabetes from 1988 to 2008 using the National Health and Nutrition Examination Survey database subdivided into 1988–1994, 1999–2004, and 2005–2008. Over time, prevalent hypertension, defined as blood pressure (BP) ≥140/≥90 mmHg or self-reported hypertension treatment, increased from 51 % to 66 %, p < 0.001. BP declined from 145.2/74.7 to 136.5/69.7, p < 0.001, among all patients with diabetes and hypertension. The reduction in BP reflected improvements in hypertension awareness (83–92 %, p < 0.001), treatment (73–87 %, p < 0.001), proportion of treated patients controlled (48–62 %, p < 0.01), and controlled to

The prevalence of high blood pressure (BP), particularly isolated systolic hypertension, rises sharply with age along with the incidence of heart failure, stroke, and coronary heart disease (CHD) (1, 2, 3). Antihypertensive treatment reduces these adverse outcomes, especially in older hypertensive patients. Unfortunately, hypertension control to less than 140/90 mmHg declines as a function of age and largely reflects inadequate control of systolic blood pressure (SBP) and largely represents the challenges in controlling systolic hypertension (4,5). Systolic hypertension dominates diastolic as a cardiovascular risk factor in older patients (1,6). The progressive rise of SBP with aging coupled with the poorer control of systolic hypertension is a major contributor to preventable cardiovascular morbidity and mortality. More than 57% of uncontrolled hypertension in the United States is accounted for by hypertensive patients 65 years of age and older, who are seen an average of four times annually for health care (7). Thus, providers have multiple opportunities to improve BP control rates through prescribing affordable and effective medication regimens and by promoting adherence.

Abdominal obesity is linked to increased non-esterified fatty acid (NEFA) concentrations and turnover that are resistant to suppression by insulin (1,2). Similarly, physical activity and maximal oxygen consumption, a marker of physical fitness, are inversely associated with plasma NEFA concentrations measured as the area under-the-curve during a standard 2-h oral glucose tolerance test (3). Familial combined hyperlipidemia, a relatively common autosomal dominant trait, is associated with high plasma NEFAs as well as greater and more prolonged elevation of NEFAs following a fat load (4). Obesity, sedentary lifestyles, and familial combined hyperlipidemia are associated with high blood pressure, abnormal glucose and lipid metabolism, and more cardiovascular events including sudden death (5, 6, 7).

This chapter focuses on nonesterified fatty acids (NEFAs), the risk factor cluster, and vascular pathophysiology. The discussion begins with an overview of the cluster and the possible pathogenetic link to the defect of insulin-mediated glucose disposal. Selected controversies in the insulin resistance—hypertension theory are addressed and another defect of insulin action, namely suppression of lipolysis and plasma NEFAs, is offered as an alternative explanation linking insulin resistance to hypertension. The emphasis moves to mechanisms by which NEFAs may modulate vascular function and structure with a focus on neurovascular tone and endothelium-dependent vasodilation. The chapter closes with thoughts on the implications of increased plasma NEFAs and their effects on neurovascular tone and endothelium-dependent vasodilation to the pathophysiology in the diabetic hypertensive.