Heart rate as a sympathetic marker during acute adrenergic challenge

Guido Grassi, Gino Seravalle, GianBattista Bolla, Fosca Quarti-Trevano, Raffaella Dell'Oro, Francesca Arenare, Giuseppe Mancia

Research output: Contribution to journalArticle

Abstract

OBJECTIVE: Previous studies have shown that heart rate has a limited value in reflecting the chronic state of adrenergic overdrive characterizing several cardiovascular diseases. Whether this also applies to the ability of heart rate to reflect acute and generalized changes in sympathetic activity is unknown. METHODS: In 20 healthy young subjects (age: 25.2 ± 1.2 years, mean ± SEM) we measured beat-to-beat blood pressure (Finapres), heart rate (HR, ECG), venous plasma norepinephrine (NE, high-performance liquid chromatography) and efferent postganglionic muscle sympathetic nerve traffic (MSNA, microneurography) at rest and during a cold pressor test and two intravenous infusions of nitroprusside at increasing doses. RESULTS: Both cold pressor test and nitroprusside infusions triggered marked and significant increases in HR, plasma NE and MSNA; blood pressure showing an increase with cold pressor test and a reduction with nitroprusside. The magnitude of the responses was greater with the higher than with the lower dose of nitroprusside. The HR changes induced by cold pressor test were not significantly related to the concomitant NE and MSNA changes (r = -0.08 and r = -0.18, P = NS). This was also the case for the lower and the higher dose of nitroprusside (NE: r = -0.11 and r = 0.08; MSNA: r = 0.01 and r = -0.11, P = NS for all). In contrast NE and MSNA changes induced by cold pressor test and by the lower and the higher dose of nitroprusside were significantly related to each other (r = 0.70, r = 0.89 and r = 0.79 respectively, P <0.01 for all). CONCLUSIONS: In a given individual, HR responses to sympathetic challenge do not quantitatively reflect the degree of acute and generalized adrenergic activation. Qualitative information on the acute adrenergic effects of given stimuli should thus be based on the assessment of NE and MSNA rather than on HR changes.

Original languageEnglish
Pages (from-to)70-75
Number of pages6
JournalJournal of Hypertension
Volume26
Issue number1
DOIs
Publication statusPublished - Jan 2008

Fingerprint

Nitroprusside
Adrenergic Agents
Heart Rate
Blood Pressure
Intravenous Infusions
Norepinephrine
Healthy Volunteers
Electrocardiography
Cardiovascular Diseases
High Pressure Liquid Chromatography
Muscles

Keywords

  • Heart rate
  • Plasma norepinephrine
  • Sympathetic activity
  • Sympathetic nerve traffic

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology

Cite this

Heart rate as a sympathetic marker during acute adrenergic challenge. / Grassi, Guido; Seravalle, Gino; Bolla, GianBattista; Quarti-Trevano, Fosca; Dell'Oro, Raffaella; Arenare, Francesca; Mancia, Giuseppe.

In: Journal of Hypertension, Vol. 26, No. 1, 01.2008, p. 70-75.

Research output: Contribution to journalArticle

Grassi, G, Seravalle, G, Bolla, G, Quarti-Trevano, F, Dell'Oro, R, Arenare, F & Mancia, G 2008, 'Heart rate as a sympathetic marker during acute adrenergic challenge', Journal of Hypertension, vol. 26, no. 1, pp. 70-75. https://doi.org/10.1097/HJH.0b013e3282f112e6
Grassi, Guido ; Seravalle, Gino ; Bolla, GianBattista ; Quarti-Trevano, Fosca ; Dell'Oro, Raffaella ; Arenare, Francesca ; Mancia, Giuseppe. / Heart rate as a sympathetic marker during acute adrenergic challenge. In: Journal of Hypertension. 2008 ; Vol. 26, No. 1. pp. 70-75.
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AU - Arenare, Francesca

AU - Mancia, Giuseppe

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N2 - OBJECTIVE: Previous studies have shown that heart rate has a limited value in reflecting the chronic state of adrenergic overdrive characterizing several cardiovascular diseases. Whether this also applies to the ability of heart rate to reflect acute and generalized changes in sympathetic activity is unknown. METHODS: In 20 healthy young subjects (age: 25.2 ± 1.2 years, mean ± SEM) we measured beat-to-beat blood pressure (Finapres), heart rate (HR, ECG), venous plasma norepinephrine (NE, high-performance liquid chromatography) and efferent postganglionic muscle sympathetic nerve traffic (MSNA, microneurography) at rest and during a cold pressor test and two intravenous infusions of nitroprusside at increasing doses. RESULTS: Both cold pressor test and nitroprusside infusions triggered marked and significant increases in HR, plasma NE and MSNA; blood pressure showing an increase with cold pressor test and a reduction with nitroprusside. The magnitude of the responses was greater with the higher than with the lower dose of nitroprusside. The HR changes induced by cold pressor test were not significantly related to the concomitant NE and MSNA changes (r = -0.08 and r = -0.18, P = NS). This was also the case for the lower and the higher dose of nitroprusside (NE: r = -0.11 and r = 0.08; MSNA: r = 0.01 and r = -0.11, P = NS for all). In contrast NE and MSNA changes induced by cold pressor test and by the lower and the higher dose of nitroprusside were significantly related to each other (r = 0.70, r = 0.89 and r = 0.79 respectively, P <0.01 for all). CONCLUSIONS: In a given individual, HR responses to sympathetic challenge do not quantitatively reflect the degree of acute and generalized adrenergic activation. Qualitative information on the acute adrenergic effects of given stimuli should thus be based on the assessment of NE and MSNA rather than on HR changes.

AB - OBJECTIVE: Previous studies have shown that heart rate has a limited value in reflecting the chronic state of adrenergic overdrive characterizing several cardiovascular diseases. Whether this also applies to the ability of heart rate to reflect acute and generalized changes in sympathetic activity is unknown. METHODS: In 20 healthy young subjects (age: 25.2 ± 1.2 years, mean ± SEM) we measured beat-to-beat blood pressure (Finapres), heart rate (HR, ECG), venous plasma norepinephrine (NE, high-performance liquid chromatography) and efferent postganglionic muscle sympathetic nerve traffic (MSNA, microneurography) at rest and during a cold pressor test and two intravenous infusions of nitroprusside at increasing doses. RESULTS: Both cold pressor test and nitroprusside infusions triggered marked and significant increases in HR, plasma NE and MSNA; blood pressure showing an increase with cold pressor test and a reduction with nitroprusside. The magnitude of the responses was greater with the higher than with the lower dose of nitroprusside. The HR changes induced by cold pressor test were not significantly related to the concomitant NE and MSNA changes (r = -0.08 and r = -0.18, P = NS). This was also the case for the lower and the higher dose of nitroprusside (NE: r = -0.11 and r = 0.08; MSNA: r = 0.01 and r = -0.11, P = NS for all). In contrast NE and MSNA changes induced by cold pressor test and by the lower and the higher dose of nitroprusside were significantly related to each other (r = 0.70, r = 0.89 and r = 0.79 respectively, P <0.01 for all). CONCLUSIONS: In a given individual, HR responses to sympathetic challenge do not quantitatively reflect the degree of acute and generalized adrenergic activation. Qualitative information on the acute adrenergic effects of given stimuli should thus be based on the assessment of NE and MSNA rather than on HR changes.

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