Marked sympathetic activation and baroreflex dysfunction in true resistant hypertension

Guido Grassi, Gino Seravalle, Gianmaria Brambilla, Claudio Pini, Marina Alimento, Rita Facchetti, Domenico Spaziani, Cesare Cuspidi, Giuseppe Mancia

Research output: Contribution to journalArticle

48 Citations (Scopus)

Abstract

Background An increase in sympathetic drive to the heart and the peripheral circulation characterizes mild and severe essential hypertension. However, it remains unsettled whether sympathetic cardiovascular influences are potentiated in true resistant hypertension (RHT).

Methods In 32 RHT patients treated with 4.6 ± 0.3 drugs (mean ± SEM) and aged 58.6 ± 2.1 years, 35 non-resistant treated hypertensives (HT) and 19 normotensive controls (NT), all age-matched with RHT, we measured clinic, 24-hour ambulatory and beat-to-beat blood pressures (BP), heart rate (HR, EKG), muscle sympathetic nerve traffic (MSNA, microneurography) and spontaneous baroreflex MSNA-sensitivity.

Results BP values were markedly greater in RHT patients than in NT and HT (172.2 ± 1.7/100.7 ± 1.2 vs 132.1 ± 1.3/82.1 ± 0.9 and 135.5 ± 1.2/83.6 ± 0.9 mm Hg, P <0.01). This was paralleled by a significant and marked increase in MSNA (87.8 ± 2.0 vs 46.8 ± 2.6 and 59.3 ± 1.7 and bursts/100 heartbeats, P <0.01). In multiple regression analysis the MSNA increase observed in RHT was significantly related to hemodynamic, hormonal and metabolic variables. It was also significantly related to plasma aldosterone values as well as spontaneous baroreflex MSNA-sensitivity, which were the variables that at the multivariate analysis were more closely related to the adrenergic activation of RHT after adjustment for confounders, including antihypertensive treatment (r2partial = 0.04405 and r2partial = 0.00878, P <0.05 for both).

Conclusions These data represent the first evidence that RHT is a state of marked adrenergic overdrive, greater for magnitude than that detectable in HT. They also suggest that impaired baroreflex mechanisms, along with hemodynamic and neurohumoral factors, may be responsible for the phenomenon.

Original languageEnglish
Pages (from-to)1020-1025
Number of pages6
JournalInternational Journal of Cardiology
Volume177
Issue number3
DOIs
Publication statusPublished - Dec 20 2014

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Baroreflex
Hypertension
Adrenergic Agents
Hemodynamics
Blood Pressure
Aldosterone
Antihypertensive Agents
Electrocardiography
Multivariate Analysis
Heart Rate
Regression Analysis
Muscles
Pharmaceutical Preparations

Keywords

  • Baroreceptors
  • Blood pressure
  • Nervous system
  • Reflex
  • Resistant hypertension

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Medicine(all)

Cite this

Marked sympathetic activation and baroreflex dysfunction in true resistant hypertension. / Grassi, Guido; Seravalle, Gino; Brambilla, Gianmaria; Pini, Claudio; Alimento, Marina; Facchetti, Rita; Spaziani, Domenico; Cuspidi, Cesare; Mancia, Giuseppe.

In: International Journal of Cardiology, Vol. 177, No. 3, 20.12.2014, p. 1020-1025.

Research output: Contribution to journalArticle

Grassi, Guido ; Seravalle, Gino ; Brambilla, Gianmaria ; Pini, Claudio ; Alimento, Marina ; Facchetti, Rita ; Spaziani, Domenico ; Cuspidi, Cesare ; Mancia, Giuseppe. / Marked sympathetic activation and baroreflex dysfunction in true resistant hypertension. In: International Journal of Cardiology. 2014 ; Vol. 177, No. 3. pp. 1020-1025.
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AU - Grassi, Guido

AU - Seravalle, Gino

AU - Brambilla, Gianmaria

AU - Pini, Claudio

AU - Alimento, Marina

AU - Facchetti, Rita

AU - Spaziani, Domenico

AU - Cuspidi, Cesare

AU - Mancia, Giuseppe

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N2 - Background An increase in sympathetic drive to the heart and the peripheral circulation characterizes mild and severe essential hypertension. However, it remains unsettled whether sympathetic cardiovascular influences are potentiated in true resistant hypertension (RHT).Methods In 32 RHT patients treated with 4.6 ± 0.3 drugs (mean ± SEM) and aged 58.6 ± 2.1 years, 35 non-resistant treated hypertensives (HT) and 19 normotensive controls (NT), all age-matched with RHT, we measured clinic, 24-hour ambulatory and beat-to-beat blood pressures (BP), heart rate (HR, EKG), muscle sympathetic nerve traffic (MSNA, microneurography) and spontaneous baroreflex MSNA-sensitivity.Results BP values were markedly greater in RHT patients than in NT and HT (172.2 ± 1.7/100.7 ± 1.2 vs 132.1 ± 1.3/82.1 ± 0.9 and 135.5 ± 1.2/83.6 ± 0.9 mm Hg, P <0.01). This was paralleled by a significant and marked increase in MSNA (87.8 ± 2.0 vs 46.8 ± 2.6 and 59.3 ± 1.7 and bursts/100 heartbeats, P <0.01). In multiple regression analysis the MSNA increase observed in RHT was significantly related to hemodynamic, hormonal and metabolic variables. It was also significantly related to plasma aldosterone values as well as spontaneous baroreflex MSNA-sensitivity, which were the variables that at the multivariate analysis were more closely related to the adrenergic activation of RHT after adjustment for confounders, including antihypertensive treatment (r2partial = 0.04405 and r2partial = 0.00878, P <0.05 for both).Conclusions These data represent the first evidence that RHT is a state of marked adrenergic overdrive, greater for magnitude than that detectable in HT. They also suggest that impaired baroreflex mechanisms, along with hemodynamic and neurohumoral factors, may be responsible for the phenomenon.

AB - Background An increase in sympathetic drive to the heart and the peripheral circulation characterizes mild and severe essential hypertension. However, it remains unsettled whether sympathetic cardiovascular influences are potentiated in true resistant hypertension (RHT).Methods In 32 RHT patients treated with 4.6 ± 0.3 drugs (mean ± SEM) and aged 58.6 ± 2.1 years, 35 non-resistant treated hypertensives (HT) and 19 normotensive controls (NT), all age-matched with RHT, we measured clinic, 24-hour ambulatory and beat-to-beat blood pressures (BP), heart rate (HR, EKG), muscle sympathetic nerve traffic (MSNA, microneurography) and spontaneous baroreflex MSNA-sensitivity.Results BP values were markedly greater in RHT patients than in NT and HT (172.2 ± 1.7/100.7 ± 1.2 vs 132.1 ± 1.3/82.1 ± 0.9 and 135.5 ± 1.2/83.6 ± 0.9 mm Hg, P <0.01). This was paralleled by a significant and marked increase in MSNA (87.8 ± 2.0 vs 46.8 ± 2.6 and 59.3 ± 1.7 and bursts/100 heartbeats, P <0.01). In multiple regression analysis the MSNA increase observed in RHT was significantly related to hemodynamic, hormonal and metabolic variables. It was also significantly related to plasma aldosterone values as well as spontaneous baroreflex MSNA-sensitivity, which were the variables that at the multivariate analysis were more closely related to the adrenergic activation of RHT after adjustment for confounders, including antihypertensive treatment (r2partial = 0.04405 and r2partial = 0.00878, P <0.05 for both).Conclusions These data represent the first evidence that RHT is a state of marked adrenergic overdrive, greater for magnitude than that detectable in HT. They also suggest that impaired baroreflex mechanisms, along with hemodynamic and neurohumoral factors, may be responsible for the phenomenon.

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KW - Blood pressure

KW - Nervous system

KW - Reflex

KW - Resistant hypertension

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