Tobacco Smoking Induces Cardiovascular Mitochondrial Oxidative Stress, Promotes Endothelial Dysfunction and Enhances Hypertension.

Tobacco Smoking Induces Cardiovascular Mitochondrial Oxidative Stress, Promotes Endothelial Dysfunction and Enhances Hypertension. Am J Physiol Heart Circ Physiol. 2019 Jan 04;: Authors: Dikalov S, Itani HA, Richmond B, Vergeade A, Rahman SMJ, Boutaud O, Blackwell T, Massion PP, Harrison DG, Dikalova AE Abstract Tobacco smoking is a major risk factor for cardiovascular disease and hypertension. It is associated with the oxidative stress and induces metabolic reprograming altering mitochondrial function. We hypothesized that cigarette smoke induces cardiovascular mitochondrial oxidative stress which contributes to endothelial dysfunction and hypertension. To test this hypothesis, we studied if scavenging of mitochondrial H2O2 in transgenic mice expressing mitochondria-targeted catalase (mCAT) attenuates the development of cigarette smoke/angiotensin II-induced mitochondrial oxidative stress and hypertension compared with wild-type mice. Two-week exposure of wild-type mice with cigarette smoke increased systolic blood pressure by 17 mm Hg which was similar to the effect of subpresssor dose of angiotensin II (0.2mg/kg/day) leading to a moderate increase to the pre-hypertensive level. Cigarette smoke exposure and low dose of angiotensin II co-operatively induced severe hypertension in wildtype mice but scavenging of mitochondrial H2O2 in mCAT mice completely prevented the development of hypertension. Cigarette smoke and angiotensin II co...
Source: American Journal of Physiology. Heart and Circulatory Physiology - Category: Physiology Authors: Tags: Am J Physiol Heart Circ Physiol Source Type: research