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      Does Smoking Act as a Friend or Enemy of Blood Pressure? Let Release Pandora's Box

      review-article
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      Cardiology Research and Practice
      SAGE-Hindawi Access to Research

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          Abstract

          In spite of the great number of observations which show the certainty of cardiovascular damage from smoking, the opinions on that are not yet unanimous. There is a discrepancy that could be attributed to the lack of reproducible data particularly in some epidemiological studies. On the contrary, experimental findings conducted on both animals and humans give evidence of exactly reproducible results of cardiovascular alterations and among these the course of Blood Pressure (BP). Findings identify an increase in BP of active smokers or non-smokers exposed to passive smoking, while a lot of others refer a lowering of BP due to smoking. This discrepancy could be explained as follows. Initially, a vasoconstriction mediated by nicotine causes acute but transient increase in systolic BP. This phase is followed by a decrease in BP as a consequence of depressant effects played chronically by nicotine itself. Simultaneously, carbon monoxide is acting directly on the arterial wall causing, in the long run, structurally irreversible alterations. At this time, there is a change in BP that increases again, and often constantly, its levels following chronic exposure. Changes in response to antihypertensive drugs have been observed in hypertensive smokers since smoking influences metabolic steps of the drugs.

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          Abnormal endothelium-dependent vascular relaxation in patients with essential hypertension.

          Endothelium regulates vascular tone by influencing the contractile activity of vascular smooth muscle. This regulatory effect of the endothelium on blood vessels has been shown to be impaired in atherosclerotic arteries in humans and animals and in animal models of hypertension. To determine whether patients with essential hypertension have an endothelium-dependent abnormality in vascular relaxation, we studied the response of the forearm vasculature to acetylcholine (an endothelium-dependent vasodilator) and sodium nitroprusside (a direct dilator of smooth muscle) in 18 hypertensive patients (mean age [+/- SD], 50.7 +/- 10 years; 10 men and 8 women) two weeks after the withdrawal of antihypertensive medications and in 18 normal controls (mean age, 49.9 +/- 9; 9 men and 9 women). The drugs were infused at increasing concentrations into the brachial artery, and the response in forearm blood flow was measured by strain-gauge plethysmography. The basal forearm blood flow was similar in the patients and controls (mean +/- SD, 3.4 +/- 1.3 and 3.7 +/- 0.8 ml per minute per 100 ml of forearm tissue, respectively; P not significant). The responses of blood flow and vascular resistance to acetylcholine were significantly reduced in the hypertensive patients (P less than 0.0001); maximal forearm flow was 9.1 +/- 5 ml per minute per 100 ml in the patients and 20.0 +/- 8 ml per minute per 100 ml in the controls (P less than 0.0002). However, there were no significant differences between groups in the responses of blood flow and vascular resistance to sodium nitroprusside. Because the vasodilator effect of acetylcholine might also be due to presynaptic inhibition of the release of norepinephrine by adrenergic nerve terminals, the effect of acetylcholine was assessed during phentolamine-induced alpha-adrenergic blockade. Under these conditions, it was also evident that the responses to acetylcholine were significantly blunted in the hypertensive patients (P less than 0.03). Endothelium-mediated vasodilation is impaired in patients with essential hypertension. This defect may play an important part in the functional abnormalities of resistance vessels that are observed in hypertensive patients.
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            Cardiovascular effects of secondhand smoke: nearly as large as smoking.

            Secondhand smoke increases the risk of coronary heart disease by approximately 30%. This effect is larger than one would expect on the basis of the risks associated with active smoking and the relative doses of tobacco smoke delivered to smokers and nonsmokers. We conducted a literature review of the research describing the mechanistic effects of secondhand smoke on the cardiovascular system, emphasizing research published since 1995, and compared the effects of secondhand smoke with the effects of active smoking. Evidence is rapidly accumulating that the cardiovascular system--platelet and endothelial function, arterial stiffness, atherosclerosis, oxidative stress, inflammation, heart rate variability, energy metabolism, and increased infarct size--is exquisitely sensitive to the toxins in secondhand smoke. The effects of even brief (minutes to hours) passive smoking are often nearly as large (averaging 80% to 90%) as chronic active smoking. The effects of secondhand smoke are substantial and rapid, explaining the relatively large risks that have been reported in epidemiological studies.
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              Passive smoking and impaired endothelium-dependent arterial dilatation in healthy young adults.

              Passive smoking has been linked to an increased risk of dying from atherosclerotic heart disease. Since endothelial dysfunction is an early feature of atherogenesis and occurs in young adults who actively smoke cigarettes, we hypothesized that passive smoking might also be associated with endothelial damage in healthy young-adult nonsmokers. We studied 78 healthy subjects (39 men and 39 women) 15 to 30 years of age (mean +/- SD, 22 +/- 4): 26 control subjects who had never smoked or had regular exposure to environmental tobacco smoke, 26 who had never smoked but had been exposed to environmental tobacco smoke for at least one hour daily for three or more years, and 26 active smokers. Using ultrasonography, we measured the brachial-artery diameter under base-line conditions, during reactive hyperemia (with flow increase causing endothelium-dependent dilatation), and after sublingual administration of nitroglycerin (an endothelium-independent dilator). Flow-mediated dilatation was observed in all control subjects (8.2 +/- 3.1 percent; range, 2.1 to 16.7) but was significantly impaired in the passive smokers (3.1 +/- 2.7 percent; range, 0 to 9; P < 0.001 for the comparison with the controls) and in the active smokers (4.4 +/- 3.1 percent; range, 0 to 10; P < 0.001 for the comparison with the controls; P = 0.48 for the comparison with the passive smokers). In the passive smokers, there was an inverse relation between the intensity of exposure to tobacco smoke and flow-mediated dilatation (r = -0.67, P < 0.001). In contrast, dilatation induced by nitroglycerin was similar in all groups. Passive smoking is associated with dose-related impairment of endothelium-dependent dilatation in healthy young adults, suggesting early arterial damage.
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                Author and article information

                Journal
                Cardiol Res Pract
                CRP
                Cardiology Research and Practice
                SAGE-Hindawi Access to Research
                2090-0597
                2011
                19 January 2011
                : 2011
                : 264894
                Affiliations
                Department of Internal Medicine, City Hospital Massa, Via Provinciale 27, 19030 Castelnuovo Magra SP, Italy
                Author notes
                *Aurelio Leone: reliol@ 123456libero.it

                Academic Editor: Undurti N. Das

                Article
                10.4061/2011/264894
                3034987
                21318159
                717487b8-ce7f-45e0-bf96-e02e41a6b3f4
                Copyright © 2011 Aurelio Leone.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 21 June 2010
                : 3 January 2011
                Categories
                Review Article

                Cardiovascular Medicine
                Cardiovascular Medicine

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