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Baroreflex Control of Sympathetic Nerve Activity in Essential and Secondary Hypertension
Abstract
Abstract —Studies performed in experimental animals and in humans have documented that high blood pressure markedly impairs baroreceptor control of heart rate. Whether a similar impairment also characterizes baroreceptor control of sympathetic activity modulating peripheral vasomotor tone is still unknown. In 28 untreated essential hypertensive subjects [14 of moderate and 14 of more severe degree, age 51.6±2.4 and 52.6±2.1 years (mean±SEM)] and in 13 untreated secondary hypertensives (renovascular or pheochromocytoma, age 50.1±4.6 years), we measured beat-to-beat arterial blood pressure (finger photoplethysmographic device), heart rate (electrocardiogram), and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during baroreceptor stimulation and deactivation induced by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Data were compared with those obtained in 15 age-matched normotensive control subjects. Muscle sympathetic nerve activity (bursts per 100 heart beats) showed a progressive and significant ( P <.01) increase from normotension (40.3±3.3) to moderate (55.6±4.1) and more severe essential hypertension (68.2±4.1), paralleling the progressive increase in blood pressure values. In contrast, muscle sympathetic nerve activity was not increased in secondary hypertensives (40.5±6.7) despite blood pressure values similar to or even greater than those of severe essential hypertensives. In both essential and secondary hypertensives, baroreceptor–heart rate control was displaced toward elevated blood pressure values and markedly impaired compared with normotensive subjects (average reduction, 38.5%). In contrast, the sympathoinhibitory and sympathoexcitatory responses to baroreceptor stimulation and deactivation were displaced toward elevated blood pressure values but similar in all groups. Thus, sympathetic activation characterizes essential but not secondary hypertension. Regardless of its nature, however, hypertension is not accompanied by an impairment of baroreceptor modulation of sympathetic activity.
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“As far as the second issue is concerned, microneurographic studies almost universally shown that sympathetic nerve traffic is potentiated in established hypertension in middle age and in elderly as well as young patients38–46.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [38]
In the citing paper
“In contrast, other microneurographic studies failed to show an increase in sympathetic nerve traffic in these forms of secondary hypertension38,54.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [38]
In the citing paper
“The sympathetic neural outflow is commonly activated also to the heart, shown with selective cardiac norepinephrine spillover measurements28, and to the skeletal muscle vasculature, demonstrated with microneurographic nerve traffic recording32,33,38–46, but it is the renal sympathetic activation which is central to hypertension pathogenesis96–97.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [38]
In the citing paper
“Despite the difficulty of establishing that every unit within a burst has a vasoconstrictor role, there is a wealth of evidence to suggest that patients with hypertension have a greater frequency of MSNA bursts than properly matched normotensive subjects (15,25–27).”
From Hypertensive left ventricular hypertrophy: relation to peripheral sympathetic drive (2001) · cites this paper as [15]
In the citing paper
“The results obtained from MSNA recordings in this study were similar to those previously published in age-comparable hypertensive subjects (15,16,25,26,28).”
From Hypertensive left ventricular hypertrophy: relation to peripheral sympathetic drive (2001) · cites this paper as [15]
In the citing paper
“Finally, and perhaps most importantly, subjects with severe hypertension in the former study had a high LVMI, whereas, in the latter study, LVH was excluded.”
From Hypertensive left ventricular hypertrophy: relation to peripheral sympathetic drive (2001) · cites this paper as [15]
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Metadata
- Authors
- Grassi, G., Cattaneo, B. M., Seravalle, G., Lanfranchi, A., & Mancia, G.
- Affiliations
- University of Milan (IT)
- Venue
- Hypertension
- Published
- 1998-01
- Volume
- 31
- Issue
- 1
- Pages
- 68-72
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2128791637
- Cited by
- 526
- References
- 26
- Citations by year
- 2026: 10 · 2025: 6 · 2024: 11 · 2023: 18 · 2022: 10 · 2021: 12 · 2020: 10 · 2019: 17 · 2018: 20 · 2017: 11 · 2016: 27 · 2015: 24 · 2014: 36 · 2013: 37 · 2012: 31
- FWCI
- 11.86
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Syncope and Autonomic Disorders
- Keywords
- baroreflex, muscle sympathetic nerve activity, essential hypertension, secondary hypertension, renovascular hypertension, pheochromocytoma, phenylephrine, sodium nitroprusside, blood pressure
- MeSH terms
- Blood Pressure, Cardiovascular Agents, Female, Heart Rate, Humans, Hypertension, Hypertension, Renovascular, Male, Middle Aged, Nitroprusside, Phenylephrine, Pheochromocytoma, Pressoreceptors, Sympathetic Nervous System, Case-Control Studies, Muscle, Skeletal
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