Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Editorial
. 2012 Mar;59(3):545-7.
doi: 10.1161/HYPERTENSIONAHA.111.182899. Epub 2012 Feb 6.

Sympathetic signatures of cardiovascular disease: a blueprint for development of targeted sympathetic ablation therapies

John W Osborn, Marcos T Kuroki
Editorial

Sympathetic signatures of cardiovascular disease: a blueprint for development of targeted sympathetic ablation therapies

John W Osborn et al. Hypertension. 2012 Mar.
No abstract available

PubMed Disclaimer

Figures

Figure 1
Figure 1
Schematic representation of the differences between the old and emerging concepts of the relationship between sympathetic nerve activity (SNA) and cardiovascular (CV) disease. The Old Concept views SNA as a single entity in which increased SNA is either “increased or decreased” and increased SNA leads to CV disease. In contrast, the Emerging Concept is that SNA is differentially regulated in a region/organ specific manner such that “disease specific sympathetic signatures” exist. See accompanying references for heart failure,, AngII-salt hypertension and human essential hypertension.
See this image and copyright information in PMC

Comment on

References

    1. Esler M. Pathophysiology of the human sympathetic nervous system in cardiovascular diseases: The transition from mechanisms to medical management. J Appl Physiol. 2010;108:227–337. - PubMed
    1. Chobanian AV. The hypertension paradox - More uncontrolled disease despite improved therapy. N Engl J Med. 2009;361:878–897. - PubMed
    1. McAllen RM, May CN. Differential drives from rostral ventrolateral medullary neurons to three identified sympathetic outflows. Am J Physiol. 1994;267:R935–R944. - PubMed
    1. Morrison SF. Differential control of sympathetic outflow. Am J Physiol. 2001;281:R683–R696. - PubMed
    1. Ramchandra R, Hood SG, Watson A, Allen AM, May CN. Central angiotensin AT1 receptor blockade decreases cardiac but not renal sympathetic nerve activity in heart failure. Hypertension. 2012 XX:XXX-XXX. - PMC - PubMed

MeSH terms

Substances