Activity of Nicotine and Inactivity of Kallikrein and Kallidin in Aggregation of Blood Platelets

Werle, E.; Schievelbein, H.

doi:10.1038/207871a0

Cited by 16 publications

(7 citation statements)

References 17 publications

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“…Other workers have reported that injection of nicotine reduces coagulation time (25,26) and causes increased aggregation of platelets in vitro (27). A similar increased thrombotic tendency of blood has been observed in man fol lowing smoking (1,2,6,7,8,12).…”

Section: Discussionsupporting

confidence: 53%

“…The mechanism of nicotine action is not completely understood, but its effect may be exerted via the blood platelet since it has been claimed that smoking accelerates thrombus formation (7) and in creases platelet adhesiveness (1,2,6,8,12). Moreover, intravenously injected nicotine has been shown to reduce coagulation time (25,26), increase the amount of platelet aggregation (27), and increase the release of 5-hydroxytryptamine as well as other biogenic amines from isolated platelets (23,24). The increased thrombotic tendency of platelets from animals after nicotine injection could result from: ( l)th e release of substances from platelets by the nicotine treatment; (2) alteration of synthesis of specific chemicals in platelets; or (3) nicotine-induced changes in plasma proteins (9).…”

Section: Introductionmentioning

confidence: 99%

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Effect of Nicotine on Clot Retraction of Rat Blood Platelets

McDonald¹,

Woodard²,

Cottrell³

1973

Pharmacology

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Clot retraction in platelet-plasma preparations was enhanced by nicotine treatment of rats. Platelets from nicotine-treated rats retracted to a greater degree if incubated in plasma from nicotine treated rats than if incubated in control plasma. Furthermore, platelets from nontreated rats retracted to a greater degree if they were incubated in plasma of nicotine-treated rats, than in plasma of nontreated rats. The results indicate that the effects of nicotine are not directly on platelets. It is concluded that the enhanced clot retraction observed in the blood of nicotine-treated animals was due to a plasma factor and not to changes in the platelets themselves.

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Section: Discussionsupporting

confidence: 53%

Section: Introductionmentioning

confidence: 99%

Effect of Nicotine on Clot Retraction of Rat Blood Platelets

McDonald¹,

Woodard²,

Cottrell³

1973

Pharmacology

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“…There should be no surprise that early work on nicotine assessed effects on platelets, not dissimilar to early headache research. Nicotine effects upon human blood platelet function were variable [22][23][24] and none. 25 Nicotine does not release serotonin from human blood platelets, 23 but it stimulates release of serotonin from them.…”

Section: Nicotine and Possible Pathophysiologic Associations With Heamentioning

confidence: 99%

Tobacco, Nicotine, and Headache

Taylor

2015

Headache

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Conflicting data support the validity of patient-reported environmental tobacco exposure as a headache trigger. Prospective controlled studies are needed, but unlikely to be performed, to determine the extent that tobacco influences the headache process, in addition to other under-recognized factors. Meanwhile, because of numerous other negative health effects, decreased tobacco exposure should be recommended to headache patients of all ages in hopes of decreasing disability and improving functionality.

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“…In a study of platelet survival, Mustard and Murphy (1963a) showed that when the subjects stopped smoking, platelet survival was prolonged. Werle and Schievelbein (1965) found that nicotine caused platelet aggregation in vitro and enhanced aggregation by ADP. Werle and Schievelbein (1965) found that nicotine caused platelet aggregation in vitro and enhanced aggregation by ADP.…”

Section: Smoking Nicotine and Carbon Monoxidementioning

confidence: 99%

Platelets, Thrombosis and Drugs

Mustard

Packham

1975

Drugs

114

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The development of thrombosis involves 4 main factors: the vessel wall, the formed elements of the blood, blood coagulation, and blood flow. In venous thrombosis, however, the major part in both the initiation and growth of thrombi is played by the platelets. In selecting drugs which inhibit platelet function it is helful to know which of the platelet reactions that contribute to thrombus formation can be inhibited by various agents. Platelets adhere to the damaged vessel wall, collagen being probably the most important constituent involved. They are then stimulated to release the contents of their storage granules. Release-inducing agents promote the discharge of adenosine diphosphate (ADP) which causes platelets in the vicinity to swell to a more spherical shape, extend pseudopods and adhere to each other. Platelet aggregation is reversible, and a number of drugs have been shown to be capable of inhibiting platelet function at various stages, both in vitro and in vivo. Adrenaline, noradrenaline, oestrogens and nicotine enhance aggregation. Drugs which inhibit platelet function include the non-steroidal anti-inflammatory drugs, the pyrimido-pyrimidines (e.g. dipyridamole), hydroxychloroquine, clofibrate, and dextran. In this review the effects of drugs which inhibit platelet function are outlined and the extent to which they can be used to influence the course of thromboembolic disease in man is discussed. It is suggested that combination of anti-platelet drugs with anticoagulants could prove clinically useful.

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Activity of Nicotine and Inactivity of Kallikrein and Kallidin in Aggregation of Blood Platelets

Cited by 16 publications

References 17 publications

Effect of Nicotine on Clot Retraction of Rat Blood Platelets

Effect of Nicotine on Clot Retraction of Rat Blood Platelets

Tobacco, Nicotine, and Headache

Platelets, Thrombosis and Drugs

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