Interaction of nicotine and prostaglandins in the cardiovascular system

Wennmalm, Åke

doi:10.1016/0090-6980(82)90029-6

Cited by 39 publications

(5 citation statements)

References 14 publications

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“…E eney (1990) has shown that one week infusion of nicotine to rabbits yields blood levels of 50 ng ml 71 and twice as high levels in cardiac tissue. Concentrations of nicotine 51 mM (160 ng/ ml 71 ) were previously found not to a ect mechanical performance, prostaglandin release or noradrenaline over¯ow in isolated non-ischaemic rabbit hearts (Wennmalm, 1982). This was con®rmed in the present trial for`physiological' concentrations of nicotine in the perfusion medium.…”

Section: Discussionsupporting

confidence: 62%

Augmented myocardial ischaemia by nicotine – Mechanisms and their possible significance

Schrör

Zimmermann

Tannhäuser

1998

British J Pharmacology

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1 To study the e ect of nicotine on the severity of experimental myocardial ischaemia, Langendor hearts of rabbits (n=7 ± 12 per group) were subjected to 2 h of low-¯ow ischaemia followed by 1 h of reperfusion. 2 Infusion of nicotine (100 ng ml 71 ) caused only minor changes in non-ischaemic conditions but a signi®cant (P50.05) increase in end-diastolic pressure (LVEDP), loss of creatine kinase (CK) and troponin (TnT) as well as increase in noradrenaline (NA) over¯ow in reperfused ischaemic hearts. 3 RT ± PCR was done on total RNA for mRNA expression of the constitutive (COX-1) and inducible cyclooxygenase (COX-2). There was no COX-2 in non-ischaemic hearts but a signi®cant expression in ischaemia (n=5) which was further increased by nicotine. These data were con®rmed at the protein level by Western blotting and additionally shown that COX-1 remained unchanged. 4 There was a marked increase in prostacyclin (PGI 2 ) and a 2 fold increase in NA over¯ow which were both stimulated by nicotine. 5 The aggravating e ects of nicotine on myocardial ischaemia (CK release) as well as the expression of COX-2 mRNA were prevented by pretreatment with the b-blocker pindolol (1 mM). 6 The data demonstrate marked deleterious actions of nicotine in reperfused ischaemic hearts. These actions are probably related to the increase in catecholamine over¯ow, are b-receptor-mediated and involve enhanced gene expression of COX-2.

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Section: Discussionsupporting

confidence: 62%

Augmented myocardial ischaemia by nicotine – Mechanisms and their possible significance

Schrör

Zimmermann

Tannhäuser

1998

British J Pharmacology

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“…There is some evidence that chronic cigarette smoking produces arterial vasoconstriction and reduces vasomotor responsiveness through inhibition of prostacyclin, thereby decreasing its anti‐aggregation effects on platelets 41–44 . These reports give evidence that cigarette smoking or nicotine perfusion in animal models reduces the synthesis of prostacyclin by vascular endothelium 45 , 46 . The cerebral microvessels are particularly active in the synthesis of prostacyclin.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Chronic Cigarette Smoking on Cerebrovascular Responsiveness to 5 Per Cent CO₂ and 100 Per Cent O₂ Inhalation

Rogers

Meyer

Shaw

et al. 1984

J American Geriatrics Society

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Effects of chronic cigarette smoking on cerebrovascular responsiveness of volunteers at risk for stroke and not at risk for stroke were evaluated by serial measurements of cerebral blood flow using the 133Xe inhalation method. Resting gray matter blood flow values (Fg) measured while breathing room air were compared with Fg values measured during inhalation of either 5 per cent CO2 in air or 100 per cent O2. Changes in Fg values during inhalation of 5 per cent CO2 were used to estimate cerebral vasodilator capacitance, and those during inhalation of 100 per cent O2 were used to estimate cerebral vasoconstrictor capacitance. Results indicated that chronic cigarette smokers have both reduced vasodilator (P less than 0.01) and reduced vasoconstrictor (P less than 0.02) capacitance when compared with nonsmokers of the same ages regardless of whether or not other risk factors for stroke were present. Vasodilator capacitance to 5 per cent CO2 inhalation was reduced among smokers compared with nonsmokers of the same age by 48 per cent in non-risk subjects and 56 per cent in risk-factored subjects, while vasoconstrictor capacitance to 100 per cent O2 inhalation among smokers was decreased by 24 per cent in non-risk subjects and 34 per cent in risk-factored subjects. In risk-factored subjects, combined effects of smoking and other risks appeared to be additive.

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“…36 The mechanism causing decreased coronary reactivity may be related to nicotine-induced reductions in vascular endothelial prostacyclin levels. [37][38][39] Cigarette smoking inhibits the reactive hyperemic response in the limb but has no effect after indomethacin administration, suggesting that smoking alters flow by prostaglandin inhibition. Nicotine has been shown to decrease prostaglandin I2 synthesis in vascular endothelium but to have no effect on thromboxane A2 production.…”

Section: Chronic Smokingmentioning

confidence: 99%

Systemic and Coronary Hemodynamic Effects of Tobacco Products on the Cardiovascular System and Potential Pathophysiologic Mechanisms

Klein¹

2021

Cardiology in Review

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Tobacco product usage is the single most preventable cause of death in the United States. Smoking promotes atherosclerosis, producing disease in the coronary arteries, the aorta, the carotid and cerebral arteries and the large arteries in the peripheral circulation. The cardiovascular consequences of tobacco products have been the subject of intensive study for several decades. Despite the overwhelming epidemiologic association between smoking and vascular disease, the pathophysiologic mechanisms by which smoking exerts its deleterious effects remain incompletely understood. This review addresses the acute and long-term systemic and coronary hemodynamic effects of tobacco, with an emphasis of the impact on coronary blood flow and pathophysiologic mechanisms.

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Interaction of nicotine and prostaglandins in the cardiovascular system

Cited by 39 publications

References 14 publications

Augmented myocardial ischaemia by nicotine – Mechanisms and their possible significance

Augmented myocardial ischaemia by nicotine – Mechanisms and their possible significance

The Effects of Chronic Cigarette Smoking on Cerebrovascular Responsiveness to 5 Per Cent CO₂ and 100 Per Cent O₂ Inhalation

Systemic and Coronary Hemodynamic Effects of Tobacco Products on the Cardiovascular System and Potential Pathophysiologic Mechanisms

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Interaction of nicotine and prostaglandins in the cardiovascular system

Cited by 39 publications

References 14 publications

Augmented myocardial ischaemia by nicotine – Mechanisms and their possible significance

Augmented myocardial ischaemia by nicotine – Mechanisms and their possible significance

The Effects of Chronic Cigarette Smoking on Cerebrovascular Responsiveness to 5 Per Cent CO2 and 100 Per Cent O2 Inhalation

Systemic and Coronary Hemodynamic Effects of Tobacco Products on the Cardiovascular System and Potential Pathophysiologic Mechanisms

Contact Info

Product

Resources

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The Effects of Chronic Cigarette Smoking on Cerebrovascular Responsiveness to 5 Per Cent CO₂ and 100 Per Cent O₂ Inhalation