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Björn Folkow Award Lecture. The sympathetic nervous system in hypertension.

Giuseppe Mancia
- 01 Dec 1997 - 
- Vol. 15, Iss: 12, pp 1553-1565
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TLDR
The contribution of this activation to the organ damage related to hypertension together with the technical progress that has recently been made on quantification of neural cardiovascular modulation, which may greatly help future studies in this area of research are outlined.
Abstract
There is clear evidence that essential hypertension is accompanied by sympathetic activation. Many studies have shown that a number of cardiovascular risk factors frequently accompanying hypertension are characterized by increased sympathetic influences as well. This paper begins with a brief overview of the origin of the sympathetic activation in essential hypertension, and then outlines the contribution of this activation to the organ damage related to hypertension together with the technical progress that has recently been made on quantification of neural cardiovascular modulation, which may greatly help future studies in this area of research.

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Sympathetic Activation in the Pathogenesis of Hypertension and Progression of Organ Damage

TL;DR: Evidence is reviewed by examining data showing that plasma norepinephrine is increased in essential hypertension and that this is also the case for systemic and regional norpinephrine spillover, as well as for the sympathetic nerve firing rate in the skeletal muscle nerve district.
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Beyond Medications and Diet: Alternative Approaches to Lowering Blood Pressure A Scientific Statement From the American Heart Association

TL;DR: It is the consensus of the writing group that it is reasonable for all individuals with blood pressure levels >120/80 mm Hg to consider trials of alternative approaches as adjuvant methods to help lower blood pressure when clinically appropriate.
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Nocturnal Continuous Positive Airway Pressure Decreases Daytime Sympathetic Traffic in Obstructive Sleep Apnea

TL;DR: CPAP treatment decreases muscle sympathetic traffic in patients with OSA, and this effect of CPAP is evident only after an extended duration of therapy.
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How to assess sympathetic activity in humans.

TL;DR: The present paper will review in detail the haemodynamic, pharmacological, biochemical, neurophysiological, neurochemical and neural imaging techniques by which sympathetic activity is assessed in humans, highlighting the main advantages and limitations of each of them.
Journal ArticleDOI

Slow Breathing Improves Arterial Baroreflex Sensitivity and Decreases Blood Pressure in Essential Hypertension

TL;DR: During spontaneous breathing, hypertensive subjects showed lower CO2 and faster breathing rate, suggesting hyperventilation and reduced baroreflex sensitivity (P<0.001 versus controls).
References
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Journal ArticleDOI

Insulin resistance in essential hypertension

TL;DR: Results provide preliminary evidence that essential hypertension is an insulin-resistant state and insulin resistance involves glucose but not lipid or potassium metabolism, is located in peripheral tissues but not the liver, is limited to nonoxidative pathways of intracellular glucose disposal, and is directly correlated with the severity of hypertension.
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Reflex Regulation of Arterial Pressure during Sleep in Man: A Quantitative Method of Assessing Baroreflex Sensitivity

TL;DR: It is concluded that the baroreceptor reflex are can be rapidly reset, particularly during sleep, and the lower arterial pressures during sleep may be actively maintained in some subjects by increased baroreflex sensitivity.
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Effect of Insulin and Glucose Infusions on Sympathetic Nervous System Activity in Normal Man

TL;DR: Insulin infusion increases sympathetic nervous system activity in the absence of changes in blood glucose in nonobese young men using glucose clamp techniques.
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Hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans

TL;DR: This study suggests that acute increases in plasma insulin within the physiological range elevate sympathetic neural outflow but produce forearm vasodilation and do not elevate arterial pressure in normal humans.
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Norepinephrine and Epinephrine Release and Adrenergic Mediation of Smoking-Associated Hemodynamic and Metabolic Events

TL;DR: Since significant smoking-associated increments, in pulse rate, blood pressure and blood lactate/pyruvate ratio, preceded measurable increments in plasma catecholamine concentrations, but were adrenergically mediated, these changes should be attributed to norepinephrine released locally from adrenergic axon terminals within the tissues rather than to increments in circulating catechlamines.
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