Search

The metabolic syndrome is a constellation of metabolic and vascular abnormalities that include insulin resistance with compensatory hyperinsulinemia, central or visceral obesity, hypertension, dyslipidemia, microalbuminuria, and oxidative stress as well as prothrombotic and inflammatory abnormalities that contribute to a hypercoagulable state and systemic endothelial dysfunction. Visceral adipose tissue is now known to secrete into the circulation a number of protein and nonprotein factors that regulate glucose metabolism in traditional insulin-sensitive tissue as well as nontraditional insulin-sensitive tissue including cardiovascular tissue. Collectively, this constellation of factors that lead to metabolic dysregulation contributes to a substantial risk for adverse cardiovascular and renal outcomes. The development of a particularly resistant form of hypertension in these individuals can be attributed to a number of factors including vasoconstriction from increased sympathetic activation, proinflammatory cytokines, and inappropriate activation of the renin-angiotensin-aldosterone system. The management of hypertension in such patients can be challenging and generally requires nonpharmacologic as well as pharmacologic interventions.

Orthostatic hypertension (OHT) is a clinically important problem increasingly recognized in persons with borderline hypertension, diabetes mellitus, and autonomic neuropathies, and in the elderly. Moreover, the association of OHT with progression of target end-organ damage, especially coronary heart disease and chronic kidney disease (CKD), and the attendant increased cardiovascular disease (CVD) and CKD risk, is gaining attention but is still underappreciated. There are various mechanisms that contribute to the development of OHT: excessive vascular adrenergic sensitivity, baroreceptor reflex abnormalities, and inappropriate activation of the renin-angiotensin-aldosterone system, which are also mechanisms that lead to cardiorenal metabolic disease (CRS). While the evidence is compelling for the clinical importance of OHT, more investigation is needed to evaluate the effects of OHT on CKD and CVD. The notion that the development of OHT is a risk factor for the development of CRS raises the need for further clinical and investigational attention to this clinical dilemma., (© 2011 S. Karger AG, Basel.)