Elevated endothelin-1 levels after cigarette smoking

Haak, Thomas; Jungmann, E.; Raab, Claudia; Usadel, K. H.

doi:10.1016/0026-0495(94)90091-4

Cited by 137 publications

(89 citation statements)

References 5 publications

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“…Some studies have found that plasma ET-1 levels are elevated in both light (1 to 10 cigarettes/d) and heavy (10 to 40 cigarettes/d) smokers in a dose-dependent fashion. 15,16 However, others have shown that smoking is associated with an acute but transient elevation in ET-1 levels 40 and that only acute, but not chronic, exposure to cigarettes results in an exaggerated vasoconstrictive response to exogenous ET-1 relative to controls. 41 The lack of significant vasodilation with BQ-123 in this study suggests that, compared with hypertension, ET-1 does not contribute substantially to vascular tone in smokers, especially via the ET A receptor.…”

Section: Et-1 and Vascular Dysfunction In Smokersmentioning

confidence: 99%

“…11,12 Risk factors for atherosclerosis are also associated with elevated plasma ET-1 levels. [13][14][15][16][17][18][19] Several studies have found that endogenous ET-1 causes vasoconstriction in the resistance vessels of subjects with hypertension. 20 -22 One group has reported that ET-1 also contributes to vascular tone in subjects with hypercholesterolemia, 23 and there are conflicting reports regarding the response to ET-1 blockade in diabetic individuals.…”

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confidence: 99%

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Endothelin-1 and Vascular Tone in Subjects With Atherogenic Risk Factors

et al. 2003

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Abstract-Endothelin-1 (ET-1) is a potent vasoconstrictor that increases vascular tone in the resistance vessels of subjects with hypertension. It is unclear whether endogenous ET-1 affects resistance-vessel function equally in patients with other cardiovascular risk factors. Vasoconstriction to ET-1 is mediated principally via the endothelin-A (ET A ) receptor on vascular smooth muscle cells. Accordingly, we used an ET A -specific antagonist, BQ-123, to test the hypothesis that endogenous ET-1 increases vascular resistance selectively in subjects with hypertension compared with other risk factors. BQ-123 was infused at 100 nmol/min for 80 minutes into the brachial artery of 10 subjects with hypertension (meanϮSEM arterial pressure, 106Ϯ5 mm Hg), 12 subjects with hypercholesterolemia (meanϮSEM total cholesterol, 7.1Ϯ0.2 mmol/L), 10 active smokers (meanϮSEM, 42Ϯ11 pack-years), and 11 healthy, age-matched individuals. ET-1 levels are elevated in patients with atherosclerosis, 10 and atherosclerotic coronary lesions exhibit enhanced ET-1-mediated vascular tone. 11,12 Risk factors for atherosclerosis are also associated with elevated plasma ET-1 levels. [13][14][15][16][17][18][19] Several studies have found that endogenous ET-1 causes vasoconstriction in the resistance vessels of subjects with hypertension. 20 -22 One group has reported that ET-1 also contributes to vascular tone in subjects with hypercholesterolemia, 23 and there are conflicting reports regarding the response to ET-1 blockade in diabetic individuals. 24,25 There have been no studies evaluating the role of endogenous ET-1 in cigarette smokers. There has also been a difference of opinion regarding the effect of ET-1 on vascular resistance in healthy individuals. 4,7,20,22,23 The fact that these observations come from several different laboratories makes it difficult to gauge whether ET-1 contributes to vascular tone equally among the various cardiac risk factors.To evaluate the relative contribution of ET-1 to vasomotor dysfunction in patients with atherogenic risk factors, we performed a single, comparative study with an ET A -selective antagonist, , to compare the activity of endogenous ET-1 in the forearm resistance vessels of subjects with hypertension, hypercholesterolemia, and cigarette smokers, relative to healthy volunteers. Methods Subject SelectionThe study population consisted of 10 subjects with hypertension (systolic blood pressure Ͼ140 mm Hg or diastolic blood pressure Ͼ90 mm Hg), 12 subjects with hypercholesterolemia (fasting cholesterol Ͼ75th percentile for age and gender), 10 active cigarette smokers (average of Ն1 pack/d for Ն3 years), and 11 healthy, age-matched controls. Subjects were recruited by advertisement in local newspapers and provided written, informed consent. Subjects were screened by history, physical examination, and routine biochemical analyses. Subjects with risk factors were excluded if they

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Section: Et-1 and Vascular Dysfunction In Smokersmentioning

confidence: 99%

mentioning

confidence: 99%

Endothelin-1 and Vascular Tone in Subjects With Atherogenic Risk Factors

et al. 2003

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“…The basal level of cortisol was reported to be higher in smokers than in non-smokers [13][14][15] . The elevation of cortisol level has been reported to be dependent on the number of cigarettes smoked per day [16][17][18] , although contradictory findings have also been reported 19) . Cigarette smoking is considered to induce frequent release of hormones that in turn lead to an altered responsiveness of the endocrine axes 8) .…”

Section: Smokingmentioning

confidence: 99%

Lifestyle, stress and cortisol response: Review II

Fukuda

Morimoto

2001

Environ Health Prev Med

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To prevent lifestyle related diseases, it is important to modify lifestyle behavior. The control of mental stress level and prevention of mental stress-related diseases have become one of the most important problems in Japan. To check mental stress level objectively during the early stage of stress-related diseases and determine appropriate coping methods, it is necessary to design a useful index for mental stress. Cortisol is a steroid hormone secreted by the adrenal cortex. This is an essential hormone to human survival, and plays a key role in adaptation to stress. In another review, we concluded that cortisol appears to be an adequate index for mental stress.However, lifestyle factors such as alcohol drinking, smoking, lack of exercise etc., are strongly associated with mental stress. Thus, in this review, we focus on the relationship between cortisol and lifestyle.The present findings suggested that lifestyle factors; smoking, alcohol drinking, exercise, sleep and nutrition are strongly associated with cortisol levels, and it may be impossible to determine whether alterations in cortisol levels are due to mental stress.It was suggested that those lifestyle effects on not only mental stress itself but also cortisol levels should be considered, when assessing mental stress by cortisol levels.

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“…Activation of the vascular endothelium by cardiovascular risk factors such as high levels of LDL and cigarette smoke exposure cause an increased production and secretion of ET-1 (Haak et al, 1994;Lubrano et al, 2008). The elevated secretion of ET-1 in connection with heart disease, hypoxia and hypertension is partly due to enhanced activity of ECE (Schiffrin et al, 1997;Davenport & Maguire, 2006).…”

Section: Endothelinsmentioning

confidence: 99%

“…Elevated plasma levels of ET-1 are seen after exposure to the risk factor cigarette smoke (Haak et al, 1994), suggesting that ET-1 contributes to the pathogenesis of CVD. Thus, pharmacological manipulation of the endothelin system might be a promising therapeutic tool for CVD.…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular risk factors regulate the expression of vascular endothelin receptors

Xu¹,

Sun²,

Edvinsson³

2010

Pharmacology & Therapeutics

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Cardiovascular disease remains as the leading cause of death in the developed world.However, there is limited knowledge about how cardiovascular risk factors actually cause vascular disease. Traditional cardiovascular risk factors include increased circulating levels of low-density lipoproteins, cigarette smoking and hypertension (both strongly related to arterial wall injury), inflammation and atherosclerosis.

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Elevated endothelin-1 levels after cigarette smoking

Cited by 137 publications

References 5 publications

Endothelin-1 and Vascular Tone in Subjects With Atherogenic Risk Factors

Endothelin-1 and Vascular Tone in Subjects With Atherogenic Risk Factors

Lifestyle, stress and cortisol response: Review II

Cardiovascular risk factors regulate the expression of vascular endothelin receptors

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