Acute Effects of Cigarette Smoking on Platelet Function and Plasma Catecholamines in Hypertensive and Normotensive Men

Abstract

In this randomized controlled crossover study essential hypertensive men (n ‫؍‬ ‫؍‬ 13) and matched normotensive controls (n ‫؍‬ ‫؍‬ 18) were examined before and during cigarette and sham smoking to assess the acute effects of smoking on platelets and plasma catecholamines. Platelet activity in vivo was determined by measurements of the released ␣-granule constituent ␤-thromboglobulin (␤-TG) in plasma and in urine. Urinary high molecular weight ␤-TG and venous plasma epinephrine increased significantly during smoking in the hypertensive group, but not among the normotensive men. Thus, cigarette smoking induces a mild platelet release reaction and also elicits a significantly higher epinephrine response in hypertensive men compared to normotensive controls. Am J Hypertens 1998;11:677-681 © 1998 American Journal of Hypertension, Ltd.KEY WORDS: ␤-Thromboglobulin, blood pressure, epinephrine, nicotine, platelet function. C igarette smoking is an important risk factor for occlusive cardiovascular disease, especially in hypertensive patients. Smoking is related to disturbances in blood platelet function.1 However, it is still not settled whether or not cigarette smoking activates platelets acutely. 2,3Cigarette smoking increases heart rate and blood pressure, probably through activation of the sympathetic nervous system. ␤-Thromboglobulin (␤-TG) is a platelet-specific protein released from the ␣-granules during the platelet release reaction and is commonly used as a marker of platelet activation. ␤-TG may, however, also be elevated by ex vivo release. To avoid such sampling-and preparation-induced elevation of plasma ␤-TG, urinary ␤-TG can be determined, as small amounts of ␤-TG are excreted by the kidneys. To minimize nonspecific interferences we measured the high molecular weight (HMW) fraction of ␤-TG in urine. The values were adjusted for urinary creatinine and reflect the platelet release reaction in vivo.5 Platelet counts and mean volumes are other relevant platelet function parameters.The aim of the present study was to examine the responses to acute effects of cigarette smoking on platelet function, plasma catecholamines, and the cardiovascular system in hypertensive men and in ageand weight-matched controls. The study design allowed us to compare baseline results between the hypertensive and normotensive group twice, 1 week apart. We also measured the plasma concentrations of fibrinopeptide A (a marker of thrombin generation), as well as nicotine and its main metabolite, cotinine.

Activity of ectonucleotidases and adenosine deaminase in rats exposed to cigarette smoke

“…Smokers with established macrovascular disease are reported to have platelet abnormalities (Mundal et al, 1998). In the present study, we did not find any change in the hydrolysis of ADP to AMP.…”

“…The reactive oxygen and nitrogen species are capable of initiating or promoting oxidative damage in biological systems (Rahman et al, 1996;Genbacev-Krtolica, 2005). Acute cigarette smoking significantly increases plasma epinephrine and induces platelet reactions, including the release of nucleotides (Mundal et al, 1998).…”

Quantitation of 3,4-Dihydroxyphenylacetaldehyde and 3,4-Dihydroxyphenylglycolaldehyde, the Monoamine Oxidase Metabolites of Dopamine and Noradrenaline, in Human Tissues by Microcolumn High-Performance Liquid Chromatography

“…DOPAL was found in only minor quantities in human plasma and urine. It should be noted, however, that tissue samples were obtained from normal controls and may not reflect levels in pathological conditions which alter levels of CA and their metabolites (21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32).…”

Telomere Length is a Biomarker of Cumulative Oxidative Stress, Biologic Age, and an Independent Predictor of Survival and Therapeutic Treatment Requirement Associated With Smoking Behavior

“…Nicotine and cotinine equipotentially reduced both leukotriene B4 production in polymorphonuclear leukocytes and thromboxane B2 production in platelet rich plasma, the inhibition increasing from 20% (0.5 nM) to 60% (0.5 mM). 44 Thus, smoking may increase platelet activation in vivo mainly in vulnerable individuals. 42 Smoking has been found to increase platelet turnover in patients with coronary artery disease (CAD), 43 but not in healthy women.…”