Functional sympatholysis in hypertension

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Sympathetic vasoconstriction is normally attenuated in exercising muscle by local changes in muscle metabolites and other substances that reduce vascular responsiveness to α-adrenergic receptor activation. Termed functional sympatholysis, this protective mechanism is thought to optimize muscle blood flow distribution to match perfusion with metabolic demand. Emerging evidence from both animal and human studies indicate that functional sympatholysis is impaired in hypertension and may constitute an important underlying cause of skeletal muscle malperfusion during exercise in this common cardiovascular condition. Findings from studies of animal models of hypertension and patients with essential hypertension will be integrated in this review to provide insight into the underlying mechanisms responsible for inappropriate sympathetic vasoconstriction in exercising muscle and the treatment options that may restore functional sympatholysis and improve muscle perfusion during exercise.

Original languageEnglish (US)
Pages (from-to)64-68
Number of pages5
JournalAutonomic Neuroscience: Basic and Clinical
Volume188
DOIs
StatePublished - Jan 1 2015

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Hypertension
Muscles
Vasoconstriction
Perfusion
Exercise
Adrenergic Receptors
Blood Vessels
Skeletal Muscle
Animal Models
Therapeutics

All Science Journal Classification (ASJC) codes

  • Endocrine and Autonomic Systems
  • Clinical Neurology
  • Cellular and Molecular Neuroscience

Cite this

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Functional sympatholysis in hypertension. / Thomas, Gail.

In: Autonomic Neuroscience: Basic and Clinical, Vol. 188, 01.01.2015, p. 64-68.

Research output: Contribution to journalArticle

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