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 language | English (US) |
|---|---|
| Pages (from-to) | 64-68 |
| Number of pages | 5 |
| Journal | Autonomic Neuroscience: Basic and Clinical |
| Volume | 188 |
| DOIs | |
| State | Published - Mar 1 2015 |
All Science Journal Classification (ASJC) codes
- Endocrine and Autonomic Systems
- Clinical Neurology
- Cellular and Molecular Neuroscience