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Updated: Aug 14, 2026

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
Published on: April 27, 2016
Endothelial control of myocardial function
1British Heart Foundation Sir Thomas Lewis Chair of Cardiology, Department of Cardiology, University of Wales College of Medicine, Cardiff, UK.
Insights
The endothelium influences heart muscle contractions by releasing agents that prolong or shorten them. Nitric oxide, released by the endothelium, abbreviates contraction by affecting calcium sensitivity.
Area of Science:
- Cardiovascular Physiology
- Endothelial Biology
- Cardiac Electrophysiology
Background:
- The endothelium, a single layer of cells lining blood vessels, plays a crucial role in regulating vascular function.
- Emerging evidence suggests the endothelium also directly influences myocardial (heart muscle) contraction.
- Understanding these endothelial mechanisms is vital for comprehending cardiac pump function.
Purpose of the Study:
- To review the phenomenon of endothelial control over myocardial contraction.
- To elucidate the agents involved and their mechanisms of action.
- To discuss the physiological, pathophysiological, and pharmacological implications.
Main Methods:
- Review of existing in vitro and in vivo studies.
- Analysis of the identified contraction-prolonging and contraction-abbreviating agents.
- Examination of the effects on myocardial cyclic GMP content and contractile protein sensitivity to calcium.
Main Results:
- Endothelium releases an unidentified agent that prolongs myocardial contraction.
- Endothelium releases nitric oxide (NO), which abbreviates myocardial contraction.
- Nitric oxide increases myocardial cyclic GMP, decreasing contractile protein sensitivity to calcium.
Conclusions:
- The endothelium actively modulates myocardial contraction through distinct signaling pathways.
- These endothelial actions have significant consequences for cardiac pump performance.
- Further research into these mechanisms may reveal new therapeutic targets for cardiovascular diseases.
Abstract:
The newly described phenomenon of endothelial control of myocardial contraction is reviewed. Endothelium both from endocardium and from coronary microvessels releases an unidentified contraction-prolonging agent and can be stimulated to release a contraction-abbreviating agent which is nitric oxide which elevates myocardial cyclic GMP content: these act by increasing and decreasing contractile protein sensitivity to cytosolic calcium respectively. The phenomenon has been confirmed in vitro and in vivo, with physiological and potential pathophysiological and pharmacological consequences for cardiac pump function.
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