Independent control of skin and muscle sympathetic nerve activity in patients with heart failure.

Middlekauff, Holly R.; Hamilton, Michèle A.; Stevenson, Lynne Warner; Mark, Allyn L.

doi:10.1161/01.cir.90.4.1794

Cited by 50 publications

(30 citation statements)

References 34 publications

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“…19,20 Taking into account that, as above mentioned, microneurographic studies have provided evidence for an increased sympathetic nerve traffic in the skeletal muscle district, the conclusion was drawn that the adrenergic overdrive characterizing HT is almost generalized to the whole cardiovascular system, the only exception being represented by the skin sympathetic district, for which no evidence of sympathetic activation has been reported in hypertensive individuals. 21 Interestingly, the pattern of the sympathetic overdrive characterizing essential HT appears to be similar to the one described in congestive heart failure, [21][22][23][24] but somewhat different from that reported in the obese normotensive state, in which no sympathetic overdrive has been documented at the level of the heart. 25 The dichotomy of the skin/muscle SNS pattern is likely to depend on the fact that whereas muscle and cardiac as well as renal sympathetic activity is under baroreflex control, 21,24 skin sympathetic nerve traffic does not depend on baroreceptor modulation.…”

Section: General Featuresmentioning

confidence: 64%

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Assessment of Sympathetic Cardiovascular Drive in Human Hypertension

2009

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Abstract-Methodological refinements in the assessment of human sympathetic cardiovascular drive have allowed throughout the years to better define the role of the sympathetic nervous system in the pathophysiology of hypertension.Earlier studies have provided evidence that indirect markers of adrenergic drive, such as plasma or urinary norepinephrine as well as heart rate, often display an increase in the hypertensive state. Direct recording of efferent postganglionic muscle sympathetic nerve traffic via microneurography and regional norepinephrine spillover technique have conclusively documented the occurrence of an adrenergic overdrive in hypertension, showing that the sympathetic activation is directly related to the severity of the hypertensive state and is widespread to different cardiovascular districts. The present review will focus on some major features of the "neuroadrenergic hypothesis of hypertension." In particular it will examine the mechanisms responsible for the adrenergic overdrive, the relationships between the sympathetic activation and the metabolic disarray of frequent detection in the hypertensive state, and the participation of neuroadrenergic factors at the development of the hypertension-related target organ damage. Further issues addressed will be the contribution of the hyperadrenergic state to the different patterns of the 24-hour blood pressure profile as well as to the day/night blood pressure variability described in the hypertensive state and the behavior of the sympathetic function in the hypertensive states complicated by the presence of other cardiovascular or metabolic disease. Finally, the clinical and therapeutic implications of the neuroadrenergic abnormalities occurring in hypertension, as well as the areas worthy of future research, will be highlighted. Key Words: sympathetic nervous system Ⅲ hypertension Ⅲ target organ damage Ⅲ 24-hour ambulatory blood pressure Ⅲ cardiometabolic risk T he role of the sympathetic nervous system (SNS) in the pathogenesis of hypertension (HT) has been remarkably changed over the past 50 years. Indeed, until a few decades ago it was believed that sympathetic neural influences were almost univocally involved in the short-term blood pressure (BP) control, with limited or even no impact at all on long-term BP regulation and development of high BP. This concept, however, has drastically changed over the past 20 years, thanks to the development of methodological approaches allowing direct assessment of systemic and regional sympathetic cardiovascular drive in humans. [1][2][3] This review will focus on the changing face of the SNS in HT. This will be done by reviewing how technical refinements in the assessment of human adrenergic function have substantially modified our thinking on this issue. The review will also examine the most recent data collected in the field, allowing to better define the role of the SNS in the pathophysiology of HT-related target organ damage, the relationships with clinic, home, and ambulatory BP as well as the links wit...

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Section: General Featuresmentioning

confidence: 64%

“…25 The dichotomy of the skin/muscle SNS pattern is likely to depend on the fact that whereas muscle and cardiac as well as renal sympathetic activity is under baroreflex control, 21,24 skin sympathetic nerve traffic does not depend on baroreceptor modulation. [21][22][23][24] …”

Section: General Featuresmentioning

confidence: 99%

Assessment of Sympathetic Cardiovascular Drive in Human Hypertension

2009

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“…[2][3][4][5] Mortality risk in HF relates to the magnitude of cardiac and peripheral sympathetic nervous system activation. 6,7 SA is present in Ͼ50% of patients with chronic stable HF.…”

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confidence: 99%

Muscle Sympathetic Nerve Activity During Wakefulness in Heart Failure Patients With and Without Sleep Apnea

et al. 2005

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Abstract-Sympathetic activation and sleep apnea are present in most patients with symptomatic systolic heart failure (HF). Acutely, obstructive and central apneas increase muscle sympathetic activity (MSNA) during sleep by eliciting recurrent hypoxia, hypercapnia, and arousal. In obstructive sleep apnea patients with normal systolic function, this increase persists after waking. Whether coexisting sleep apnea augments daytime MSNA in HF is unknown. We tested the hypothesis that its presence exerts additive effects on MSNA during wakefulness. Overnight sleep studies and morning MSNA recordings were performed on 60 subjects with ejection fraction Ͻ45%. Of these, 43 had an apnea-hypopnea index Ն15 per hour. Subjects with and subjects without sleep apnea were similar for age, ejection fraction, HF etiology, body mass index, blood pressure, and heart rate.

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“…MSNA is chronically elevated in patients with heart failure, obesity, and essential hypertension; however, SSNA is not elevated in these conditions compared with healthy controls (8,23). The mechanisms underlying the nonuniform distribution of sympathetic activity in these conditions is not certain, but it is thought to be due to impaired baroreflex sensitivity.…”

Section: Discussionmentioning

confidence: 97%

“…A dissociation between MSNA and SSNA has been found in other disease states characterized by chronic sympathetic overactivity, including heart failure, essential hypertension, and obesity (8,23). In these conditions, heightened MSNA was found, without concomitant elevations in SSNA.…”

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confidence: 95%