Hypertension, Vol 18, 709-721, Copyright © 1991 by American Heart Association
OG Kuchel and GA Kuchel
Dopamine, an ancestral catecholamine, is physiologically natriuretic and
vasodilating, thus essentially protecting against hypertension. Its actions
are overshadowed by the opposite effects of its main biological partner,
norepinephrine, and this is accentuated with aging. Clinical observations
combined with molecular biology approaches to catecholamine-synthesizing
and catecholamine-metabolizing enzymes and receptors permit the
identification of some inborn defects. Subtle changes in the
dopamine-norepinephrine balance may account for the enhanced peripheral
noradrenergic activity seen in the setting of decreased dopaminergic
activity in advanced age. These changes may contribute to the diminished
ability of the aged kidney to excrete a salt load, as well as to the
finding that systolic blood pressure increases with age in populations with
a high, but not in those with a low, intake of salt. The attainment of
advanced age in Western societies with adverse lifestyle changes (mental
rather than physical stress, excess salt intake, overeating, sedentarism)
appears to facilitate the development of hypertension. The adaptation to
all the preceding lifestyle changes necessitates an increased dopamine
generation, which may initially compensate to maintain appropriate
natriuresis and vasodilation since many patients with initial borderline
essential hypertension express their sympathetic hyperfunction, in addition
to increased norepinephrine release, by excessive dopamine release.
However, the progression of hypertension is accompanied by a peripheral
dopaminergic deficiency and diminished ability to excrete salt. This may
represent an eventual inadequacy of a phylogenetically redundant system
resulting in decreased natriuresis and vasodilation and may account for the
responsiveness of established chronic hypertension to salt restriction,
diuretics, and dopaminomimetic medication.
ARTICLES
Peripheral dopamine in pathophysiology of hypertension. Interaction with aging and lifestyle
Clinical Research Institute of Montreal, Quebec, Canada.
This article has been cited by other articles:
![]() |
C. Zeng, H. Sanada, H. Watanabe, G. M. Eisner, R. A. Felder, and P. A. Jose Functional genomics of the dopaminergic system in hypertension Physiol Genomics, November 17, 2004; 19(3): 233 - 246. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Efendiev, C. E. Budu, A. R. Cinelli, A. M. Bertorello, and C. H. Pedemonte Intracellular Na+ Regulates Dopamine and Angiotensin II Receptors Availability at the Plasma Membrane and Their Cellular Responses in Renal Epithelia J. Biol. Chem., August 1, 2003; 278(31): 28719 - 28726. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. S. Goldstein, K. J. Swoboda, J. M. Miles, S. W. Coppack, A. Aneman, C. Holmes, I. Lamensdorf, and G. Eisenhofer Sources and Physiological Significance of Plasma Dopamine Sulfate J. Clin. Endocrinol. Metab., July 1, 1999; 84(7): 2523 - 2531. [Abstract] [Full Text] |
||||
![]() |
H. Brismar, M. Asghar, R. M. Carey, P. Greengard, and A. Aperia Dopamine-induced recruitment of dopamine D1 receptors to the plasma membrane PNAS, May 12, 1998; 95(10): 5573 - 5578. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Ricci, E. Bronzetti, P. Mulatero, M. Schena, F. Veglio, and F. Amenta Dopamine D3 Receptor in Peripheral Mononuclear Cells of Essential Hypertensives Hypertension, December 1, 1997; 30(6): 1566 - 1571. [Abstract] [Full Text] |
||||
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1991 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |