Blood Pressure Reduction is Associated With the Changes in Oxidative Stress and Endothelial Activation in Hypertension, Regardless of Antihypertensive Therapy

Abstract

Background/Aims: Hypertensive patients present with increased oxidative stress and frequently receive angiotensin II (ANGII) receptor type I blockers (ARB) for blood pressure (BP) reduction. Recent studies revealed an important role of ANGII in maintaining vascular oxidative homeostasis, including sustaining normal sodium dismutase activity. This study aimed to investigate the effects of antihypertensive therapy and also vitamin C/E supplementation on BP, oxidative stress and endothelial activation in patients with essential hypertension. Methods: Newly discovered patients received ARB/olmesartan or the Ca²⁺-channel blocker (CCB)/amlodipine, and additionally vitamin C/E or placebo throughout weeks 9-16. ELISA was used to determine 8-iso-prostaglendin F2-alpha (8iPGF2α) and endothelial activation markers. Results: In both groups BP was normalized during first 8 weeks of therapy. Vitamins C/E had no additional BP-lowering effect. The vitamins C/E supplementation was not effective in reducing absolute values of 8iPGF2α; however; the magnitude of 8iPGF2α reduction was significantly greater in patients taking vitamins C/E in the CCB group. Although plasma 8iPGF2α positively correlated to BP, a significant decrease occurred during an additional 8 weeks of treatment. There were no changes in endothelial activation markers related to the specific action of ARB or CCB. Conclusions: Present study suggests that observed oxidative stress is a consequence of hypertension. BP reduction is associated with the observed decrease in oxidative stress and changes in endothelial activation regardless of antihypertensive therapy.

Taurine Ameliorates Thyroid Hypofunction and Renal Injury in L-NAME-Induced Hypertensive Rats

“…Moreover, increased free radical production represents a major mechanism that often leads to a reduction in NO availability due to endothelial dysfunction in hypertension [57]. The association between hypertension and oxidative stress has been demonstrated in hypertensive patients [13,58]. The renal damage observed in the present investigation is associated with the increased production of oxidative stress evidenced by decreased GSH levels and elevated H 2 O 2 and LPO levels in the kidneys of L-NAME-treated rats.…”

Chronic treatment with paeonol improves endothelial function in mice through inhibition of endoplasmic reticulum stress-mediated oxidative stress

“…Oxidative stress can impact vascular tone leading to endothelial dysfunction [39, 40]. ROS promotes vascular cell proliferation and migration, inflammation and apoptosis, as well as extracellular matrix alterations [41, 42]. Inhibition of ER stress in hypertension improved macrovascular endothelial function by transforming growth factor-β1 (TGF-β1)-dependent mechanism and microvascular endothelial function by an oxidative stress-dependent mechanism [36].…”

Oxidative Stress: A Unifying Paradigm in Hypertension

“…18 These processes cause oxidative damage of cells and tissues with consequent endothelial dysfunction, renal injury, and cardiovascular remodelling, processes that are attenuated by angiotensin-converting enzyme inhibitors, ROS scavengers, and Nox inhibitors. 98 Moreover, in mice deficient in Nox2 and p47phox, the blood pressureeelevating effect of Ang II is blunted. 99,100 These findings confirm the central role of ROS in Ang IIemediated vascular dysfunction and hypertension.…”