Published online before print October 1, 2007, doi: 10.1161/HYPERTENSIONAHA.107.096974
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Hypertension. 2007;50:835.)
© 2007 American Heart Association, Inc.
Editorial Commentaries |
Qualitative Assessment of Sympathetic Neural Drive in Cardiometabolic Disease
A New Challenge
From the Clinica Medica, Università Milano-Bicocca, Ospedale San Gerardo; Centro Interuniversitario di Fisiologia Clinica e Ipertensione; and Istituto Auxologico Italiano, Milan, Italy.
Correspondence to Guido Grassi, Clinica Medica, Ospedale S Gerardo, Via Pergolesi 33, 20052 Milan, Italy. E-mail guido.grassi@unimib.it
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Much information has been collected over the past few years on the main features of neuroadrenergic abnormalities that characterize cardiovascular disease. We learned, eg, that in a number of pathological states adrenergic influences lose their homeostatic regulatory function and become "less sympathetic," not only favoring the development of the disease itself but also contributing to its clinical progression. We also learned that elevated circulating plasma norepinephrine levels do not invariably reflect sympathetic activation and that complex but accurate methodologic approaches to quantify neuroadrenergic drive should be of help in dissecting the peripheral (reduced clearance and or reuptake of norepinephrine) versus the central (increased in central sympathetic outflow) origin of the sympathetic activation characterizing a given physiological or pathophysiological condition. Other key findings of recent investigations in the field of neural cardiovascular control should not be forgotten. They include, eg, the evidence that sympathetic influences on cardiac, renal, thermoregulatory, and metabolic function are not independent entities but rather complex phenomena integrating each other in a "neurally exchanging network." They also include the evidence that, in several cardiovascular and noncardiovascular diseases, therapeutic counterbalance of adrenergic overdrive may be clinically relevant for reducing cardiovascular risk, improving cardiovascular function, and possibly retarding the progression and favoring the regression of the end-organ damage. This therapeutic goal is based on a well-documented rationale, namely the evidence that in a number of diseases (heart failure, acute myocardial infarction, stroke, and renal failure) sympathetic activation has proven clinical and prognostic relevance.1
In the present issue of Hypertension,
Related Article:
Hypertension 2007 50: 862-868.
This article has been cited by other articles:
 |
|
 |
|
  G. L. Rosenthal Insulin Resistance Predicts Elevated Nighttime Blood Pressure in Obese Children and Adolescents AAP Grand Rounds, June 1, 2008; 19(6): 67 - 68. [Full Text] [PDF]
|
|