(Hypertension. 1999;34:461-465.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
From the Cattedra di Medicina Interna, Università di Milano, Ospedale S. Gerardo dei Tintori, Monza, and Centro di Fisiologia Clinica e Ipertensione, IRCCS, Milano, Italy.
Correspondence to Professor Giuseppe Mancia, Cattedra di Medicina Interna, Università di Milano, Ospedale S. Gerardo, Via Donizetti 106, 20052 Monza, Italy.
AbstractPheochromocytoma is usually characterized by a marked increase in peripheral catecholamine secretion. Whether this is accompanied by an alteration in central sympathetic drive has not been clarified. In 6 patients with adrenal pheochromocytoma (mean±SEM age, 49.3±7.2 years), we measured systolic and diastolic blood pressure (photoplethysmographic device), heart rate (ECG), venous plasma catecholamines (high-performance liquid chromatography), and postganglionic muscle sympathetic nerve activity (microneurography) before and 78.3±13 days after surgical removal of the tumor. In each experimental session, measurements were performed during (1) a 60-minute resting period to compare several values of sympathetic nerve traffic at similar blood pressures before and after surgery and (2) voluntary end-expiratory apnea, ie, a maneuver inducing sympathetic activation. Tumor removal significantly (P<0.05 at least) reduced plasma catecholamines, blood pressure, and heart rate. In contrast, muscle sympathetic nerve activity was significantly (P<0.01) increased, both when quantified as bursts per minute (from 28.1±5.7 to 54.3±7.5) and as bursts per 100 heartbeats (from 33.4±5.6 to 65.1±6.5). This was also the case when data were evaluated in periods of 2 experimental sessions characterized by similar diastolic blood pressure values. The apnea maneuver induced sympathetic nerve traffic responses that were significantly (P<0.05) greater after surgery than before surgery. These data provide the first direct evidence that in pheochromocytoma central sympathetic outflow is markedly reduced and that this reduction cannot be ascribed to a reflex inhibitory response to elevated blood pressures. It is likely that this sympathoinhibition is rather due to a central depression of sympathetic outflow induced by high circulating catecholamines.
Key Words: nervous system, sympathetic catecholamines nervous system, autonomic
This article has been cited by other articles:
![]() |
M. Sesay, P. Tauzin-Fin, P. Gosse, P. Ballanger, and P. Maurette Real-Time Heart Rate Variability and Its Correlation with Plasma Catecholamines During Laparoscopic Adrenal Pheochromocytoma Surgery Anesth. Analg., January 1, 2008; 106(1): 164 - 170. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. E. Lohmeier, T. M. Dwyer, D. A. Hildebrandt, E. D. Irwin, M. A. Rossing, D. J. Serdar, and R. S. Kieval Influence of Prolonged Baroreflex Activation on Arterial Pressure in Angiotensin Hypertension Hypertension, November 1, 2005; 46(5): 1194 - 1200. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. E. Lohmeier, D. A. Hildebrandt, S. Warren, P. J. May, and J. T. Cunningham Recent insights into the interactions between the baroreflex and the kidneys in hypertension Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2005; 288(4): R828 - R836. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. Taneja, A. Diedrich, B. K. Black, D. W. Byrne, S. Y. Paranjape, and D. Robertson Modafinil Elicits Sympathomedullary Activation Hypertension, April 1, 2005; 45(4): 612 - 618. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. L. Bravo and R. Tagle Pheochromocytoma: State-of-the-Art and Future Prospects Endocr. Rev., August 1, 2003; 24(4): 539 - 553. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. E. Lohmeier, J. R. Lohmeier, A. Haque, and D. A. Hildebrandt Baroreflexes prevent neurally induced sodium retention in angiotensin hypertension Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2000; 279(4): R1437 - R1448. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. Mancia, G. Grassi, C. Giannattasio, and G. Seravalle Sympathetic Activation in the Pathogenesis of Hypertension and Progression of Organ Damage Hypertension, October 1, 1999; 34(4): 724 - 728. [Abstract] [Full Text] [PDF] |
||||
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1999 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |