Hypertension: Basics Concepts and the Evolving Role of Novel Treatments
Hypertension, a major cardiovascular risk factor, is the primarily cause of mortality worldwide. A large body of evidence indicates that patients with essential hypertension, and even more those with complicated hypertension, are characterized by endothelial dysfunction due to impaired nitric oxide (NO) availability secondary to oxidative stress production. Therefore, a dysfunctioning endothelium is an early marker in the development of cardiovascular events. This observation suggest that treatment strategies that improve endothelial function would exert beneficial effects in hypertensive subjects, and may also help to prevent the development of hypertension and its cardiovascular complications. Part I of the present review describes the etiology of hypertension as well as the role of NO in the physio-pathology of the endothelium whereas in Part II, we are reporting novel treatments e.g. beta-blockers, ACE inhibitors, calcium channel antagonists, NO therapies, selective inhibitors of PDE Type 5, statins and regular aerobic physical exercise to the event to improve or restore endothelial function. In the near future, large scale clinical trials are required to demonstrate that treatment of endothelial dysfunction can lead to better prognosis in patients with essential hypertension.
Keywords: Hypertension, blood pressure, endothelial dysfunction, nitric oxide and therapies, cardiovascular risk factor, oxidative stress, beta-blockers, ACE inhibitors, calcium channel antagonists, coronary heart disease, systemic hemodynamics, endothelin, vasoconscrictor prostanoids, angiotensin II, superoxide anions, high intracellular levels of free ca2+, endothelium-derived contracting factors, atherosclerosis, diabetes, cGMP-dependent protein kinase I, (ROS)-producing enzymes, NADPH oxidase, xanthine oxidase, mitochondrial superoxide producing enzymes, guanylate cyclase, human cardiovascular system, Nebivolol, L-arginine-NO pathway, captopril, Calcium Channel Antagonists, NO synthase, cyclic guanosine monophosphate, Statins, Reactive Nitrogen Species, Reactive Oxygen Species
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