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Abstract-Vascular upregulation of nitric oxide (NO) is an adaptive response to increased blood pressure that may help in the prevention of end-organ damage. Differences in cardiovascular and renal morbidity and mortality in hypertensive patients may result, at least in part, from individual variations in endothelial 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 an important component. In hypertension, salt sensitivity, whether primary (ie, certain populations in the United States and Japan) or secondary (ie, aging, 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 diabetes and atherosclerosis, NO-dependent vascular relaxation is impaired and can be restored by decreasing the synthesis and/or blocking the action of Ang II. An understanding of the relations between hypertension, cardiovascular risk factors, end-organ damage, and the NO-Ang II axis leads one to believe that the combination of therapeutic agents capable of reinstating the homeostatic balance of these vasoactive molecules within the vessel wall would be most effective in preventing or arresting end-organ disease. Key Words: endothelium Ⅲ angiotensin II Ⅲ nitric oxide Ⅲ stress T he role of the renin-angiotensin (Ang) II system, particularly of Ang II, holds high interest in the areas of cardiovascular and renal physiology and pathology. Of most interest, after the discovery of the beneficial effects of Ang II-converting enzyme (ACE) inhibitors in hypertension and cardiovascular and renal disease, are Ang II's nonhemodynamic effects 1,2 rather than its better-known hemodynamic effect as a vasopeptide. The L-arginine/nitric oxide (NO) pathway, particularly NO as an endothelial-derived relaxing factor, has also been an area of keen interest. [3][4][5][6] The interactions of and balance between Ang II and NO are of key importance in cardiovascular and renal injury and are the focus of this review. Indeed, the presence or the relative bioavailability of either one can make it either injurious or protective of target organs (Figure 1).Research shows general agreement that functionally complete local renin-angiotensin systems are operative within organs/tissues. 7-9 The systems act in both autocrine and paracrine fashion, 7,8 potentially accounting for the local actions of Ang II and NO; angiotensin II and NO interact at the level of the endothelium, which is where they undergo the final step of synthesis as well as at the level of vascular smooth muscle cells, mesangial cells, and matrix. The endothelial cells contain ACE, which converts Ang I to Ang II. NO has been shown to downregulate the synthesis of ACE 10 in the endothelium, as well as Ang II type 1 receptors (AT 1 ) in vascular smooth muscle cells, thus having the poten...
Abstract-Vascular upregulation of nitric oxide (NO) is an adaptive response to increased blood pressure that may help in the prevention of end-organ damage. Differences in cardiovascular and renal morbidity and mortality in hypertensive patients may result, at least in part, from individual variations in endothelial 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 an important component. In hypertension, salt sensitivity, whether primary (ie, certain populations in the United States and Japan) or secondary (ie, aging, 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 diabetes and atherosclerosis, NO-dependent vascular relaxation is impaired and can be restored by decreasing the synthesis and/or blocking the action of Ang II. An understanding of the relations between hypertension, cardiovascular risk factors, end-organ damage, and the NO-Ang II axis leads one to believe that the combination of therapeutic agents capable of reinstating the homeostatic balance of these vasoactive molecules within the vessel wall would be most effective in preventing or arresting end-organ disease. Key Words: endothelium Ⅲ angiotensin II Ⅲ nitric oxide Ⅲ stress T he role of the renin-angiotensin (Ang) II system, particularly of Ang II, holds high interest in the areas of cardiovascular and renal physiology and pathology. Of most interest, after the discovery of the beneficial effects of Ang II-converting enzyme (ACE) inhibitors in hypertension and cardiovascular and renal disease, are Ang II's nonhemodynamic effects 1,2 rather than its better-known hemodynamic effect as a vasopeptide. The L-arginine/nitric oxide (NO) pathway, particularly NO as an endothelial-derived relaxing factor, has also been an area of keen interest. [3][4][5][6] The interactions of and balance between Ang II and NO are of key importance in cardiovascular and renal injury and are the focus of this review. Indeed, the presence or the relative bioavailability of either one can make it either injurious or protective of target organs (Figure 1).Research shows general agreement that functionally complete local renin-angiotensin systems are operative within organs/tissues. 7-9 The systems act in both autocrine and paracrine fashion, 7,8 potentially accounting for the local actions of Ang II and NO; angiotensin II and NO interact at the level of the endothelium, which is where they undergo the final step of synthesis as well as at the level of vascular smooth muscle cells, mesangial cells, and matrix. The endothelial cells contain ACE, which converts Ang I to Ang II. NO has been shown to downregulate the synthesis of ACE 10 in the endothelium, as well as Ang II type 1 receptors (AT 1 ) in vascular smooth muscle cells, thus having the poten...
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