Hypertension and cardiovascular risk factors - Role of the angiotensin II-nitric oxide interaction

Vascular upregulation of nitric oxide (NO) is an adaptive response to incre ased blood pressure that may help in the prevention of end-organ damage. Di fferences in cardiovascular and renal morbidity and mortality in hypertensi ve patients may result, at least in part, from individual variations in end othelial function in response to the hemodynamic workload of hypertension. A functional feedback balance exists between both angiotensin (Ang) II and NO under normal conditions. The NO-Ang II imbalance may not explain all the vascular pathophysiology of hypertension, but it certainly appears to be a n important component. In hypertension, salt sensitivity, whether primary ( ie, certain populations in the United States and Japan) or secondary (ie, a ging, type II diabetes), appears to be a marker of increased cardiovascular and renal risk that is often linked to a decreased bioactivity of NO. In d iabetes and atherosclerosis, NO-dependent vascular relaxation is impaired a nd can be restored by decreasing the synthesis and/or blocking the action o f Ang II. An understanding of the relations between hypertension, cardiovas cular risk factors, end-organ damage, and the NO-Ang II axis leads one to b elieve that the combination of therapeutic agents capable of reinstating th e homeostatic balance of these vasoactive molecules within the vessel wall would be most effective in preventing or arresting end-organ disease.