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Query: UMLS:C0242339 (dyslipidemia)
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Pathophysiological effects of the autonomic nervous system are clearly seen in young patients with a high cardiac output and borderline hypertension. As the hypertension progresses, there is a change from the hyperkinetic circulation in borderline hypertension to the increased vascular resistance seen in established hypertension. This hemodynamic transition is caused by decreased beta-adrenergic responsiveness and decreased end-diastolic distension of the heart combined with an increased alpha-adrenergic responsiveness of the resistance vessels. In parallel, the sympathetic tone decreases in the course of hypertension. This transition in sympathetic tone can be explained by the hypothesis of the 'blood pressure seeking properties of the brain'. The central nervous system 'seeks' to maintain a higher pressure. When vascular overresponsiveness sets in, less sympathetic drive is needed to maintain a neurogenic hypertension. Sympathetic overactivity in borderline hypertension is associated with overweight subjects, insulin resistance and dyslipidemia. This suggests a new area of research to investigate the basis of metabolic abnormalities in hypertension.
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PMID:Changing role of the autonomic nervous system in human hypertension. 209 97

Considerable progress has been made in our understanding of the role of the nervous system in human hypertension. The evidence for a widespread autonomic abnormality in the early phases of hypertension is overwhelming and excessive sympathetic activity is consistently present in such patients since their childhood. The enhanced sympathetic tone in hypertension is associated with the metabolic syndrome of insulin resistance and dyslipidemia. Multiple mechanisms by which sympathetic overactivity could cause both hypertension and the metabolic syndrome have been documented. Furthermore, the excessive sympathetic tone is conducive to coronary heart disease through its association with high hematocrit values and with excessive platelet aggregability. Surprisingly, the myth that patients with neurogenic hypertension have a benign prognosis continues to persist. Much of the misunderstanding stems from the idea that patients with neurogenic hypertension, commonly called "white coat" or borderline hypertension, do not develop established hypertension. There is no support for such an assessment; in fact, patients with neurogenic hypertension are at a high risk of future accelerated hypertension. Another misunderstanding relates to differences in hemodynamics between neurogenic and established hypertension. It is true that patients with neurogenic hypertension initially show an increase of cardiac output. However, this later evolves into a classic picture of established high resistance hypertension. The hemodynamic transition is secondary to a decrease in cardiac responsiveness and an increase in vascular responsiveness over the course of hypertension. With passage of time, vascular reactivity increases, yet sympathetic tone tends to decrease. This can be explained by the "blood pressure seeking behavior of the central nervous system." In hypertension, the central nervous system appears to seek a higher blood pressure level and, as the vasculature becomes hyperresponsive, less sympathetic tone is needed to maintain the elevated blood pressure. This decrease of sympathetic tone in later phases of hypertension should not be viewed as a normalization, since sympathetic tone in relationship to vascular hyperresponsiveness remains excessive and the central nervous system maintains a crucial role in sustaining high blood pressure in hypertension.
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PMID:Sympathetic overactivity in hypertension. A moving target. 893 44