Essential hypertension, or hypertension of unknown cause, accounts for more than 90% of cases of hypertension. In the last decade, significant advances have occurred in our understanding of the presence and nature of endothelial dysfunction in a number of cardiovascular conditions, including hypertension. Endothelial dysfunction contributes to the underlying disease process of a number of conditions, including essential hypertension, hypercholesterolemia, atherosclerosis, diabetes mellitus, congestive heart failure, and pulmonary hypertension. Endothelium-derived nitric oxide (NO) is recognized as an important mediator of endothelium-dependent vascular relaxation, and a defect in the endothelium-derived NO system-possibly decreased synthesis and/or release of NO by endothelial cells is now known to cause the abnormal response to acetylcholine in hypertensive vessels and to account at least in part for the increased vascular resistance observed in hypertension. These findings have contributed to our understanding of endothelial dysfunction in essential hypertension and have pointed out distinctions between the mechanisms leading to this vascular abnormality in hypertensive patients.
Endothelial dysfunction in hypertension may lead to the development of novel therapeutic strategies to reduce the vascular complications associated with the hypertensive process.
Endothelial cells are strategically located between the circulating blood and the vascular smooth muscle. Endothelium-delivered vasodilators include prostacyclin, bradykinin, endothelium derived hyperpolarising factor, and nitric oxide. These effects are counterbalanced by endothelial vasoconstrictors, such as reactive oxygen species, endothelin-1, and angiotensin II, which exert pro-thrombotic, inflammatory, and growth promoting properties. Cardiovascular risk factors cause cardiovascular disease by causing endothelial dysfunction, thus, modern therapeutic strategies focus on preserving or restoring endothelial integrity. Angiotensin converting enzyme (ACE) inhibitors prolong the half-life of bradykinin and stabilize the bradykinin receptor linked to formation of nitric oxide. Chronic ACE inhibition improves endothelial function in patients with cardiovascular risk. This may explain why patients treated with ACE inhibitors experience a greater cardiovascular benefit than is attributable to the decrease in blood pressure.
Cardiovascular protection aims at preventing vascular disease and its associated complications. ACE inhibition is shown to be beneficial in cardiovascular diseases, independent of the etiology of the disease.
CONCLUSION:
The endothelium is an important target organ in cardiovascular protection, and treatment with ACE inhibitors restores diminished NO bioavailability, thus restoring endothelium function in various diseases.
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