Increased vascular contractility in isolated vessels from cigarette smoking rats is mediated by basal endothelin release

Rahman, Mohammad Mizanur; Elmi, Shahrzad; Chang, Thomas K. H.; Bai, Na; Sallam, Nada; Lemos, Virgı́nia S.; Moien‐Afshari, Farzad; Laher, Ismail

doi:10.1016/j.vph.2006.06.006

Cited by 28 publications

(35 citation statements)

References 88 publications

(58 reference statements)

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“…It has been reported that chronic exposure CS exposure can increase systemic oxidative stress [1], alter NO bioavailability [23], cause endothelial dysfunction [24,25], and influence the levels of other major risk factors, such as blood pressure [26]. Our data show that short-term exposure to CS induces a significant increase in SBP.…”

Section: Discussionsupporting

confidence: 61%

Short-Term Systemic Effects of Nose-Only Cigarette Smoke Exposure in Mice: Role of Oxidative Stress

Nemmar

Raza

Subramaniyan

et al. 2013

Cell Physiol Biochem

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Background/Aims: Long–term cigarette smoking (CS) is a major risk factor for respiratory and cardiovascular diseases, and is also known to adversely affect other organs. However, data on the systemic effects of short-term CS exposure (STCSE) are scarce. Presently, using a nose-only exposure system, we evaluated the systemic effects of STCSE in mice. Methods: We assessed the effects of CS generated by 9 consecutive cigarettes per day for 4 days in a nose-only exposure system on cardiovascular, hepatic and renal endpoints evaluated on day 5 in mice. Control mice were exposed to air only. Results: CS significantly increased systolic blood pressure and decreased total nitric oxide plasma concentration. Circulating platelets and erythrocyte numbers were also increased. However, STCSE did not significantly increase thrombosis in pial arterioles and venules. STCSE significantly raised plasma alanine aminotransferase and gamma glutamyl transpeptidase activities, but did not affect urea or creatinine concentrations. Interestingly, while STCSE enhanced the production of reactive oxygen species in heart and kidney and lipid peroxidation in heart, liver and kidneys, it also enhanced the antioxidant activity of superoxide dismutase, probably indicating that STCSE causes adaptive reactions to counterbalance the potentially damaging action of oxygen radicals induced by STCSE. Conclusion: These results suggest that STCSE causes blood pressure increase, hepatotoxicity and oxidative stress in the heart, liver and the kidneys. These data provide information on the initial steps leading to the systemic effects of STCSE, a stage at which the diseases may likely be reversed.

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Section: Discussionsupporting

confidence: 61%

Short-Term Systemic Effects of Nose-Only Cigarette Smoke Exposure in Mice: Role of Oxidative Stress

Nemmar

Raza

Subramaniyan

et al. 2013

Cell Physiol Biochem

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“…Recent studies have confirmed that the increased ET-1 release in cigarette smoking is associated with an increased arterial tone and reduced vasorelaxation. 22 This study did not show a significant difference in endothelial function of saphenous vein between ex-and nonsmokers. Previous studies assessing endothelial function in the pulmonary vasculature have shown a similar result, with recovery of endothelial function after cessation of smoking.…”

Section: Discussioncontrasting

confidence: 61%

Smoking Impairs Endothelial Function in Human Saphenous Vein in an Ex Vivo Model

Sharif

Bayraktutan

Arya

et al. 2009

Annals of Vascular Surgery

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“…In fact, exhaled breath condensate and circulating ET-1 levels are increased in COPD patients with PH, and both are correlated with pulmonary systolic pressure [5]. Furthermore, animals exposed to CS show an increase in basal ET-1 levels and vascular contractility, which may contribute to the pulmonary pathophysiology associated with CS [26]. Recent studies performed on rat arteries originating from various tissues, such as brain, mesentery and kidney, conclude that CSE upregulates ETB and ETA expression by a mechanism that implicates the activation or phosphorylation of ERK1/2, p38, JNK, protein kinase (PK)C and NF-kB [9][10][11].…”

Section: Discussionmentioning

confidence: 99%

Bosentan inhibits cigarette smoke-induced endothelin receptor expression in pulmonary arteries

Milara

Gabarda²,

Juan³

et al. 2011

Eur Respir J

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The endothelin (ET) system contributes to lung vascular tension and remodelling in smokers and chronic obstructive pulmonary disease (COPD) patients.This study examined the effect of cigarette smoke (CS) on ET receptor A (ETA) and B (ETB) expression in human pulmonary artery smooth muscle cells (HPASMCs) and human small intrapulmonary arteries, as well as their functional consequences.CS extract (CSE) increased ETA and ETB expression in HPASMCs and small intrapulmonary arteries, which was attenuated by bosentan, the ETA antagonist BQ123 and the ETB antagonist BQ788, and by blocking ET-1 with a monoclonal antibody against ET-1, suggesting a feed-forward mechanism mediated by ET-1 release. ET receptor (ETR) antagonism attenuated the CSE-induced HPASMC proliferation. Furthermore, CSE exposure increased the acute ET-1-induced small intrapulmonary artery contraction, which was attenuated by bosentan, BQ123 and BQ788. Pulmonary arteries from smokers and COPD patients showed a higher expression of ETA and ETB than those of nonsmoker patients.These results show a novel mechanism by which ETR blockade attenuates CS-induced ETR overexpression and, subsequently, small intrapulmonary artery tension. These data may be of potential value to explain therapeutic effects of bosentan in some forms of disproportionate pulmonary hypertension in COPD patients.KEYWORDS: Bosentan, cigarette smoke, endothelin receptor, human pulmonary artery smooth muscle cells, precision-cut lung slice P ulmonary hypertension (PH) is a relatively common form of cigarette smoke (CS)-induced lung disease. PH develops in ,6% of subjects with chronic obstructive pulmonary disease (COPD) but is present in ,40% of patients with a forced expiratory volume in 1 s of ,1 L [1, 2]. The pathogenesis of PH in COPD is unclear. Current studies suggest that PH is caused by the direct effects of CS on the intrapulmonary vessels by the secretion of a number of vasoconstrictive/proliferative peptides, such as endothelin (ET) or vascular endothelial growth factor, which subsequently contribute to vascular remodelling and the development of PH [3]. The circulating levels of ET-1 are elevated after exposure to CS in humans [4] and it has been shown that ET-1 correlates with pulmonary systolic pressure in COPD patients with PH [5], suggesting that ET-1 is involved in CS-induced vascular remodelling. ET-1 activates two receptors, ETA and ETB, which are located in pulmonary artery smooth muscle cells (PASMCs), whilst exclusively ETB are present in endothelial cells. Both ETA and ETB mediate proliferation and contractility in PASMCs from small pulmonary arteries, while endothelial ETB mediates vasodilation in normal pulmonary arteries. ETB upregulation has been observed in human blood vessels from patients with ischaemic heart disease [6], hypertension [7] and severe PH [8]. More recently, it has been shown that CS extract (CSE) induces ETA and ETB overexpression in resistant cerebral arteries from rats by a mechanism implicating the activation of the intracellular m...

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Increased vascular contractility in isolated vessels from cigarette smoking rats is mediated by basal endothelin release

Cited by 28 publications

References 88 publications

Short-Term Systemic Effects of Nose-Only Cigarette Smoke Exposure in Mice: Role of Oxidative Stress

Short-Term Systemic Effects of Nose-Only Cigarette Smoke Exposure in Mice: Role of Oxidative Stress

Smoking Impairs Endothelial Function in Human Saphenous Vein in an Ex Vivo Model

Bosentan inhibits cigarette smoke-induced endothelin receptor expression in pulmonary arteries

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