Chronic cigarette smoking causes hypertension, increased oxidative stress, impaired NO bioavailability, endothelial dysfunction, and cardiac remodeling in mice

M. A Hassan Talukder, Wesley M. Johnson, Saradhadevi Varadharaj, Jiarui Lian, Patrick N. Kearns, Mohamed A. El-Mahdy, Xiaoping Liu, Jay L. Zweier

Research output: Contribution to journalArticle

Abstract

Cigarette smoking is a major independent risk factor for cardiovascular disease. While the association between chronic smoking and cardiovascular disease is well established, the underlying mechanisms are incompletely understood, partly due to the lack of adequate in vivo animal models. Here, we report a mouse model of chronic smoking-induced cardiovascular pathology. Male C57BL/6J mice were exposed to whole body mainstream cigarette smoke (CS) using a SCIREQ "InExpose" smoking system (48 min/day, 5 days/wk) for 16 or 32 wk. Age-matched, air-exposed mice served as nonsmoking controls. Blood pressure was measured, and cardiac MRI was performed. In vitro vascular ring and isolated heart experiments were performed to measure vascular reactivity and cardiac function. Blood from control and smoking mice was studied for the nitric oxide (NO) decay rate and reactive oxygen species (ROS) generation. With 32 wk of CS exposure, mice had significantly less body weight gain and markedly higher blood pressure. At 32 wk of CS exposure, AChinduced vasorelaxation was significantly shifted to the right and downward, left ventricular mass was significantly larger along with an increased heart-to-body weight ratio, in vitro cardiac function tended to be impaired with high afterload, white blood cells had significantly higher ROS generation, and the blood NO decay rate was significantly faster. Thus, smoking led to blunted weight gain, hypertension, endothelial dysfunction, leukocyte activation with ROS generation, decreased NO bioavailability, and mild cardiac hypertrophy in mice that were not otherwise predisposed to disease. This mouse model is a useful tool to enable further elucidation of the molecular and cellular mechanisms of smoking-induced cardiovascular diseases.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume300
Issue number1
DOIs
StatePublished - Jan 2011
Externally publishedYes

Fingerprint

Biological Availability
Nitric Oxide
Oxidative Stress
Smoking
Hypertension
Smoke
Tobacco Products
Reactive Oxygen Species
Cardiovascular Diseases
Weight Gain
Blood Vessels
Leukocytes
Body Weight
Cardiomegaly
Inbred C57BL Mouse
Vasodilation
Chronic Disease
Animal Models
Air
Pathology

Keywords

  • Blood pressure
  • Cardiovascular function
  • Chronic cigarette smoke exposure
  • Nitric oxide
  • Reactive oxygen species

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)
  • Cardiology and Cardiovascular Medicine

Cite this

Chronic cigarette smoking causes hypertension, increased oxidative stress, impaired NO bioavailability, endothelial dysfunction, and cardiac remodeling in mice. / Talukder, M. A Hassan; Johnson, Wesley M.; Varadharaj, Saradhadevi; Lian, Jiarui; Kearns, Patrick N.; El-Mahdy, Mohamed A.; Liu, Xiaoping; Zweier, Jay L.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 300, No. 1, 01.2011.

Research output: Contribution to journalArticle

Talukder, M. A Hassan ; Johnson, Wesley M. ; Varadharaj, Saradhadevi ; Lian, Jiarui ; Kearns, Patrick N. ; El-Mahdy, Mohamed A. ; Liu, Xiaoping ; Zweier, Jay L. / Chronic cigarette smoking causes hypertension, increased oxidative stress, impaired NO bioavailability, endothelial dysfunction, and cardiac remodeling in mice. In: American Journal of Physiology - Heart and Circulatory Physiology. 2011 ; Vol. 300, No. 1.
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AU - Kearns, Patrick N.

AU - El-Mahdy, Mohamed A.

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