Heart rate as a sympathetic marker during acute adrenergic challenge

G Grassi, G Seravalle, GB Bolla… - Journal of …, 2008 - journals.lww.com
G Grassi, G Seravalle, GB Bolla, F Quarti-Trevano, R Dell'Oro, F Arenare, G Mancia
Journal of hypertension, 2008journals.lww.com
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: 25.2ą1.2
years, meanąSEM) we measured beat-to-beat blood pressure (Finapres), heart rate (HR,
ECG), venous plasma norepinephrine (NE, high-performance liquid chromatography) and …
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: 25.2ą1.2 years, meanąSEM) 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.
Lippincott Williams & Wilkins