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Coronary endothelial dysfunction in the hypertensive patient: from myocardial ischemia to heart failure
1Division of Cardiovascular Diseases, Mayo Clinic and Foundation, Rochester, MN 55905, USA.
Insights
Cardiovascular diseases involve an imbalance between nitric oxide (NO) and endothelin (ET). This review highlights how impaired NO and increased ET contribute to endothelial dysfunction in heart conditions.
Area of Science:
- Cardiovascular Science
- Endothelial Biology
- Vascular Physiology
Background:
- The endothelium regulates vascular tone via nitric oxide (NO) and endothelin (ET).
- Dysfunctional NO generation and elevated ET levels are observed in cardiovascular diseases like atherosclerosis, heart failure, and hypertension.
- An imbalance between NO and ET is implicated in altered vascular tone.
Purpose of the Study:
- To review the current understanding of NO and ET roles in cardiovascular pathophysiology.
- To focus on the contribution of these mediators to coronary endothelial dysfunction.
Main Methods:
- Literature review of existing research on nitric oxide and endothelin.
- Analysis of studies investigating endothelial function in cardiac diseases.
- Synthesis of data on NO/ET balance and vascular tone.
Main Results:
- Cardiovascular diseases are associated with reduced NO bioavailability and increased ET production.
- This NO/ET imbalance is a key factor in the vascular tone alterations seen in these conditions.
- Coronary endothelial dysfunction is significantly influenced by this mediator imbalance.
Conclusions:
- The balance between NO and ET is critical for maintaining normal vascular tone.
- Therapeutic strategies targeting NO and ET pathways may be beneficial for cardiovascular diseases.
- Further research into coronary endothelial dysfunction and NO/ET interplay is warranted.
Abstract:
The endothelium modulates vascular tone by the release of vasodilator and vasoconstrictor substances, among them nitric oxide (NO) and endothelin (ET). Abnormalities in NO generation have been demonstrated in various cardiac pathophysiological states, specifically atherosclerotic vascular disease, congestive heart failure, and essential and pulmonary hypertension. Moreover, increases in plasma ET has been reported as well in these disease states. When these observations are taken together, these states may be characterized by an attenuated release of NO, whereas the release of ET is augmented. An imbalance between NO and ET may contribute to the alteration in vascular tone characteristic of cardiovascular disease. The following review summarizes the present knowledge of the role of NO and ET in such disease processes with a major focus on coronary endothelial dysfunction.