1992
DOI: 10.1097/00004872-199205000-00014
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Persistent blood pressure increase induced by heavy smoking

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Cited by 279 publications
(161 citation statements)
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“…The association between smoking and elevated TER alb in our NIDDM patients has also been demonstrated in non-diabetic subjects [52]. Several factors may contribute such as carbon monoxide [53], nicotine [54], and acute intermittent blood pressure elevation in association with smoking [55].…”
Section: Discussionsupporting
confidence: 66%
“…The association between smoking and elevated TER alb in our NIDDM patients has also been demonstrated in non-diabetic subjects [52]. Several factors may contribute such as carbon monoxide [53], nicotine [54], and acute intermittent blood pressure elevation in association with smoking [55].…”
Section: Discussionsupporting
confidence: 66%
“…Experimental studies in men and animals have shown that smoking or nicotine administration produces small acute increases in blood pressure and heart rate, presumably due to release of catecholamines (United States Department of Health and Education and Welfare; Public Health Service 1979). This acute blood pressure increase has been attributed to smoking-induced vasoconstriction and accelerated heart rate (Aronow et al 1971;Cellina et al 1975;Cryer et al 1976;Benowitz et al 1982;Benowitz et al 1984;De Cesaris et al 1991;De Cesaris et al 1992;Groppelli et al 1992). Moreover, Istvan et al (1999) reported that the level of salivary cotinine, a nicotine metabolite, was positively correlated with blood pressure in long-term smokers, suggesting that long-term nicotine exposure might be related to modest elevations in blood pressure.…”
Section: Discussionmentioning
confidence: 99%
“…The non-modifiable factors include age (Yamaguchi et al, 2005) and sex (with women generally having higher resting HR when compared with men) (Stolarz et al, 2003). The modifiable (physiologic) factors include (i) circadian rhythm (HR is usually lower during sleep) (Ben-Dov et al, 2007); (ii) BP (HR is positively associated with BP) (Zhang & Kesteloot, 1999); (iii) physical activity (training reduces the resting HR (Borresen & Lambert, 2008); (iv) mental stress (increases catecholamines, and hence HR and BP) (Carter & Ray, 2009); (v) smoking (increases HR and BP) (Groppelli et al, 1992); (vi) alcohol consumption (increases HR) (Kloner & Rezkalla, 2007) and (vii) excess body weight, (increases HR) (S. Julius et al, 2000). The importance of the resting HR as a prognostic factor and potential therapeutic target is not yet generally accepted, even though recent large epidemiologic studies have confirmed earlier studies that showed resting HR to be an independent predictor of CV and all-cause mortality in men and women with and without diagnosed CVD.…”
Section: Heart Ratementioning
confidence: 99%