The Protective Effects of Angiotensin II Blockade with Olmesartan Medoxomil on Resistance Vessel Remodeling (The VIOS study)

Abstract

The suppression of the RAS by the blockade of angiotensin II type 1 (AT(1)) receptors may demonstrate remodeling effects on the ubiquitous small resistance vessels similar to that seen in the myocardium and renal glomeruli, thus affording more complete end-organ protection.

The Role of Beta-Blockers as First-Line Therapy in Hypertension

“…In a prospective study on a small group of untreated hypertensive patients randomized to atenolol or amlodipine, after 1 year of treatment, the amlodipine group saw a correction of altered resistance artery structure (on gluteal resistance vessels) and tended to improve endothelial function, whereas patients treated with atenolol did not show any vascular benefit given a similar BP control as the amlodipine group [31]. Similar results were obtained with an angiotensin II blocker, olmesartan [32], which also showed the ability to significantly reduce carotid plaque volume in comparison to atenolol, in the presence of similar reductions of intima-media thickness [33]. Furthermore, in another study, switching from a BB to irbesartan resulted in correction of previously persistently altered vascular structure and endothelial dysfunction, thus suggesting a structural and endothelial protective effect of angiotensin-1 receptor antagonists [34].…”

The blocking of angiotensin II type 1 receptor and RhoA/Rho kinase activity in hypertensive patients: Effect of olmesartan medoxomil and implication with cardiovascular-renal remodeling

“…15 Moreover, the treatment of these patients with olmesartan increased the protein expression of heme oxygenase-1, 15 a potent antioxidant and anti-inflammatory protein, 16,17 and the number of cEPCs and reduced cEPCs apoptosis in addition to increase the level of calcitonin generelated peptide, 18 a vasorelaxant that prevents cEPCs senescence, reverses Ang II-induced senescence of EPCs and reduces blood pressure in spontaneously hypertensive rats. 19 Furthermore, although indirectly, the vasoprotective, antiinflammatory and anti-atherosclerotic effects of olmesartan shown in humans in the European Trial on Olmesartan and Pravastatin in Inflammation and Atherosclerosis (EUTOPIA), Vascular Improvement with Olmesartan medoxomil Study (VIOS), Multicenter Olmesartan Atherosclerosis Regression Evaluation (MORE) and Impact of OLmesartan on progression of coronary atherosclerosis: Evaluation by IntraVascular UltraSound (OLIVUS) clinical trials [23][24][25][26] can be linked with an inhibitory effect on oxidative stress and oxidative stress signaling as a mechanism involved in the effects of olmesartan observed in these studies. Given these effects of olmesartan on oxidative stress and on the improvement of endothelial dysfunction including inflammatory processes mediated by Ang II and given that RhoA/Rho kinase activation, as mentioned above, is mainly involved in the Ang II signaling following Ang II AT1R activation including oxidative stress, [1][2][3]9 it comes as no surprise that olmesartan may be able to downregulate the RhoA/Rho kinase pathway via AT1R blockade and reduction of oxidative stress effects.…”

Oxidative Dna Damage in Newly Diagnosed and Untreated Patients with Isolated High Blood Pressure: The Acute Effect of Olmesartan

“…Deneysel modellerde olmesartanın kan basıncı düşürücü etkileri dışında önemli pleiotropik etkileri olduğu gözlenmiştir. Totale yakın nefrektomize ratlarda ilerleyici glomerüler hasarı azaltır (13), hipoksi ilişkili sol ventriküler yeniden yapılanma üzerine olumlu etki gösterir (14), ileri evre hipertansif diyastolik kalp yetersizliğinde iyileşme sağlar (15), akut viral miyokarditte miyokardiyal hasarlanmayı azaltır (16) ve son olarak aort ve böbrekte yüksek düzeyde proteinli beslenmeyle ilişkili ortaya çıkan OS'yi düzelttiği belirlenmiştir (17 Olmesartanın birincil hipertansif insanlarda, arterlerde olumlu bir gelişme olarak, duvar/lümen oranında düşme sağladığı VIOS çalışmasında gösterilmiştir (18). Bu etkinin hangi mekanizma ile gerçekleştiği net olarak bilinmemektedir.…”