(Hypertension. 2001;38:286.)
© 2001 American Heart Association, Inc.
Scientific Contributions |
From Clinica Medica, Università Milano-Bicocca, Ospedale San Gerardo (G.G., G.M.), Monza (Milan); Centro di Fisiologia Clinica e Ipertensione (G.G., C.T., G.S., G.B., A.P., G.M.), IRCCS; and Istituto Auxologico Italiano (G.G., C.T., G.S., G.M.), Milan, Italy.
Correspondence to Prof Giuseppe Mancia, Clinica Medica, Ospedale S. Gerardo dei Tintori, Via Donizetti 106, 20052 Monza (Milan), Italy.
Abstract Congestive heart failure is characterized by a sympathetic activation that is coupled with a baroreflex impairment. Whether these alterations are affected by clonidine is unknown. In 26 normotensive patients age 58.0±1.1 years (mean±SEM) affected by congestive heart failure (New York Heart Association functional class II or III) and treated with furosemide and enalapril, we measured mean arterial pressure, heart rate, venous plasma norepinephrine, and muscle sympathetic nerve traffic (microneurography) at rest and during baroreceptor stimulation and deactivation caused by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Measurements were repeated after a 2-month administration of transdermal clonidine patch (14 patients) or placebo (12 patients) according to a double-blind, randomized sequence. Clonidine caused a slight, nonsignificant reduction in mean arterial pressure and heart rate without affecting exercise capacity and echocardiographically determined left ventricular ejection fraction. In contrast, both plasma norepinephrine and sympathetic nerve traffic were significantly reduced (-46.8% and -26.7%, respectively; P<0.01 for both). This reduction was coupled with no change in cardiac and sympathetic baroreflex responses. Transdermal placebo administration for a 2-month period did not affect any of the above-mentioned variables. Thus, in congestive heart failure patients who are undergoing conventional drug treatment, chronic clonidine administration exerts marked sympathoinhibitory effects without adversely affecting cardiac functions and clinical state. Whether this leads to further therapeutic benefits remains to be tested.
Key Words: nervous system, sympathetic nervous system, autonomic baroreceptors clonidine heart failure
This article has been cited by other articles:
![]() |
J. Neumann, G. Ligtenberg, I. H.T. Klein, P. Boer, P. L. Oey, H. A. Koomans, and P. J. Blankestijn Sympathetic Hyperactivity in Hypertensive Chronic Kidney Disease Patients Is Reduced During Standard Treatment Hypertension, March 1, 2007; 49(3): 506 - 510. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Neumann, G. Ligtenberg, L. Oey, H. A. Koomans, and P. J. Blankestijn Moxonidine Normalizes Sympathetic Hyperactivity in Patients with Eprosartan-Treated Chronic Renal Failure J. Am. Soc. Nephrol., November 1, 2004; 15(11): 2902 - 2907. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. S. Akers and L. A. Cassis Presynaptic modulation of evoked NE release contributes to sympathetic activation after pressure overload Am J Physiol Heart Circ Physiol, June 1, 2004; 286(6): H2151 - H2158. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Aggarwal, M. D. Esler, M. J. Morris, G. Lambert, and D. M. Kaye Regional Sympathetic Effects of Low-Dose Clonidine in Heart Failure Hypertension, March 1, 2003; 41(3): 553 - 557. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. M. Small, L. E. Wagoner, A. M. Levin, S. L.R. Kardia, and S. B. Liggett Synergistic Polymorphisms of {beta}1- and {alpha}2C-Adrenergic Receptors and the Risk of Congestive Heart Failure N. Engl. J. Med., October 10, 2002; 347(15): 1135 - 1142. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. S. Floras The "Unsympathetic" Nervous System of Heart Failure Circulation, April 16, 2002; 105(15): 1753 - 1755. [Full Text] [PDF] |
||||
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2001 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |