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Bradykinin increases myocardial contractility: relation to the Gregg phenomenon
1Department of Medicine, University of California, San Diego, La Jolla 92037.
The American Journal of Physiology
|June 1, 1991
Summary
Bradykinin (BK) enhances myocardial shortening by increasing coronary blood flow, independent of neural pathways. This effect may contribute to stimulating cardiac nerves during heart ischemia.
Area of Science:
- Cardiovascular Physiology
- Cardiac Electrophysiology
- Neurocardiology
Background:
- Bradykinin (BK) is present in the heart during ischemia.
- BK activates cardiac afferent nerves, potentially acting as nociceptors.
Purpose of the Study:
- To investigate if bradykinin (BK) alters myocardial shortening.
- To determine if BK-induced changes in myocardial shortening contribute to afferent nerve stimulation.
Main Methods:
- In open-chest dogs, BK was injected into the left anterior descending (LAD) coronary artery.
- Myocardial wall motion, blood pressure, heart rate, left ventricular pressure, and LAD coronary flow were monitored.
- Segment gauges measured wall motion, and nerve integrity was assessed via vagotomy and stellate ganglionectomy.
Main Results:
- BK injection increased regional myocardial shortening in the LAD region, preceding systemic blood pressure changes.
- The response correlated with increased coronary flow and was mimicked by adenosine, suggesting a flow-mediated effect.
- The observed changes were not abolished by vagotomy or stellate ganglionectomy, indicating a non-neural mechanism.
Conclusions:
- Bradykinin (BK) enhances regional myocardial shortening primarily by increasing coronary blood flow (Gregg phenomenon).
- Systemic hypotension induced by BK also affects global ventricular function and myocardial shortening.
- BK-induced alterations in myocardial shortening may play a role in stimulating cardiac afferent nerves.