Nicotine, the Heart and Blood Vessels

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1. Research at a Glance
2. The Papers
3. PubMed Topic Searches
4. More Nicotine Research
5. Connections
6. Featured Videos

Research at a Glance

What kind of study each paper on this page is, and when the papers were published. Hover over a bar for its count.

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The Papers (30)

Newest first. Study types on this page — Human trial: 5 · Human observational study: 1 · Review: 10 · Animal study: 10 · Cell study: 4. Each summary is written from the paper’s own abstract; follow the PubMed link for the full record.

Impact of Smokeless Oral Nicotine Products on Cardiovascular Disease: Implications for Policy, Prevention, and Treatment: A Policy Statement From the American Heart Association

Review, 2025. This is a policy statement from a major heart-health organization reviewing what is known about smokeless oral nicotine products such as nicotine pouches, gums, lozenges, tablets, and gummies, and their effect on heart health. It reports that these products are addictive and have mixed effects on cardiovascular risk markers, with some types linked to higher death rates in people who already have heart or blood-vessel disease. It also notes that no data yet exist on the heart or health risks of newer nicotine pouches specifically, and that synthetic nicotine's cardiovascular effects have not been well studied. The statement calls for stronger public policies to prevent people from starting these products and to support quitting.

Dennison Himmelfarb CR, Benowitz NL, Blank MD et al. (2025). Impact of Smokeless Oral Nicotine Products on Cardiovascular Disease: Implications for Policy, Prevention, and Treatment: A Policy Statement From the American Heart Association. Circulation. — PubMed PMID: 39624904 · doi:10.1161/CIR.0000000000001293

Nicotine Ingestion Reduces Heart Rate Variability in Young Healthy Adults

Human trial, 2022. This randomized controlled trial gave 4 mg of nicotine by mouth to 80 young, healthy non-smokers (40 men and 40 women) and measured heart rate variability, a marker of how flexibly the heart's rhythm adjusts. Nicotine reduced heart rate variability in both men and women, and the size of the effect did not differ between the sexes. The authors concluded that nicotine at doses of 4 mg or more is harmful to the heart of young people.

Guo QN, Wang J, Liu HY et al. (2022). Nicotine Ingestion Reduces Heart Rate Variability in Young Healthy Adults. Biomed Res Int. — PubMed PMID: 35028314 · doi:10.1155/2022/4286621

Long-term cerebrovascular dysfunction in the offspring from maternal electronic cigarette use during pregnancy

Animal study, 2021. Researchers exposed pregnant rats to e-cigarette vapor for 1 hour a day, 5 days a week, using liquid with either no nicotine or 18 mg/mL nicotine, and compared them with rats breathing ordinary air. Birth weight and weaning weight did not differ. In the offspring, a main brain artery widened 51% to 56% less in response to a signal from its inner lining, at 1, 3 and 7 months of age. This happened equally with and without nicotine, so the authors concluded that the vapor's base liquid, not nicotine, caused the problem. These results are in rats only.

Burrage EN, Aboaziza E, Hare L et al. (2021). Long-term cerebrovascular dysfunction in the offspring from maternal electronic cigarette use during pregnancy. Am J Physiol Heart Circ Physiol. — PubMed PMID: 34170194 · doi:10.1152/ajpheart.00206.2021

Nicotine: Regulatory roles and mechanisms in atherosclerosis progression

Review, 2021. This review looks at how nicotine itself may drive atherosclerosis, the build-up of fatty plaque in the artery walls. It notes that tobacco smoke contains more than 7000 chemicals and says nicotine is closely tied to the disease. According to the authors, nicotine acts on nicotinic acetylcholine receptors in nerve and non-nerve tissues. Through these receptors it raises growth factors and inflammation, damages the cells lining blood vessels and the smooth muscle cells and macrophages in the vessel wall, increases reactive oxygen species, disturbs fat metabolism and activates immune cells. The authors also discuss blocking nicotine receptors and using exosomes, tiny particles released by cells, as possible future ways to prevent smoking-related atherosclerosis.

Fu X, Zong T, Yang P et al. (2021). Nicotine: Regulatory roles and mechanisms in atherosclerosis progression. Food Chem Toxicol. — PubMed PMID: 33774093 · doi:10.1016/j.fct.2021.112154

Nicotine exacerbates atherosclerosis through a macrophage-mediated endothelial injury pathway

Animal study, 2021. This study looked at how nicotine might speed up atherosclerosis, the build-up of fatty plaque in the arteries. In 100 patients with coronary heart disease, smokers had more plaque and higher levels of inflammation signals than non-smokers. In immune cells called macrophages grown in the lab, and in mice prone to artery disease that were fed a high-fat diet, nicotine raised oxidative stress and switched on an inflammation pathway (TXNIP/NLRP3) that makes macrophages die in an inflammatory way and damages the cells lining the blood vessels. In the mice, blocking this pathway or giving the antioxidant N-acetyl-cysteine reversed these effects, but the step-by-step mechanism was shown only in cells and animals.

Mao C, Li D, Zhou E et al. (2021). Nicotine exacerbates atherosclerosis through a macrophage-mediated endothelial injury pathway. Aging (Albany NY). — PubMed PMID: 33626512 · doi:10.18632/aging.202660

Endothelial to mesenchymal transition contributes to nicotine-induced atherosclerosis

Animal study, 2020. Researchers gave nicotine in drinking water for 12 weeks to mice bred to develop hardened arteries, and also exposed human artery-lining cells to nicotine in the lab. Nicotine-treated mice developed larger artery plaques, and the cells lining their blood vessels began turning into a different, scar-like cell type, with a weakened barrier function. This change ran through a nicotine receptor called alpha7 and a chain of signals inside the cell, and blocking the receptor reduced the change and the plaques in the mice. These findings come from mice and lab-grown cells only, not from people.

Qin W, Zhang L, Li Z et al. (2020). Endothelial to mesenchymal transition contributes to nicotine-induced atherosclerosis. Theranostics. — PubMed PMID: 32373212 · doi:10.7150/thno.42470

Nicotine in Senescence and Atherosclerosis

Review, 2020. This review looked at published research on how nicotine and its main breakdown product, cotinine, may affect the heart and blood vessels, apart from the other contents of cigarette smoke. The authors propose that nicotine raises inflammation and oxidative stress through an enzyme called NADPH oxidase 1, and that this pushes smooth muscle cells in artery walls into an aged, non-dividing state called senescence. They say a build-up of these aged cells in the cap covering an artery plaque makes the plaque less stable and worsens atherosclerosis. They conclude that nicotine, and probably cotinine, harm atherosclerosis, but this is a hypothesis drawn from a review of earlier studies, not a new study.

Centner AM, Bhide PG, Salazar G (2020). Nicotine in Senescence and Atherosclerosis. Cells. — PubMed PMID: 32331221 · doi:10.3390/cells9041035

Electronic cigarettes and cardiovascular health: what do we know so far?

Review, 2019. This review looks at what is known about how e-cigarettes affect the heart and blood vessels. The authors note that nicotine is the main biologically active substance in e-cigarette vapor, while the cancer-causing chemicals and burning by-products found in tobacco smoke are very low or undetectable. They describe how tobacco cigarettes harm the heart through inflammation, oxidative damage, clogged arteries, blood clots and nervous-system activation, and they discuss which of these ways of causing harm may also apply to e-cigarette use. They conclude that although e-cigarettes are generally thought to be safer than tobacco cigarettes, their overall effects on heart health are still uncertain, and they discuss the debate between rising e-cigarette use among young people and the use of e-cigarettes to help people quit smoking.

MacDonald A, Middlekauff HR (2019). Electronic cigarettes and cardiovascular health: what do we know so far?. Vasc Health Risk Manag. — PubMed PMID: 31417268 · doi:10.2147/VHRM.S175970

Nicotine promotes atherosclerosis via ROS-NLRP3-mediated endothelial cell pyroptosis

Animal study, 2018. Researchers tested nicotine in mice bred to develop clogged arteries and fed a high-fat diet, and in human artery-lining cells grown in the lab. In the mice, nicotine led to larger artery plaques and more inflammatory signals. In the cells, nicotine set off an inflammation pathway that made the cells die in an inflammatory way, and blocking reactive oxygen species with N-acetyl-cysteine stopped this cell death. These results come only from mice and lab-grown cells, not from people.

Wu X, Zhang H, Qi W et al. (2018). Nicotine promotes atherosclerosis via ROS-NLRP3-mediated endothelial cell pyroptosis. Cell Death Dis. — PubMed PMID: 29416034 · doi:10.1038/s41419-017-0257-3

Cardiovascular toxicity of nicotine: Implications for electronic cigarette use

Review, 2016. This review looks at whether nicotine itself harms the heart and blood vessels, as part of the debate over the risks of electronic cigarettes. It explains that nicotine has drug effects that could contribute to sudden heart events and faster buildup of artery plaque, the kind seen in cigarette smokers. Studies of nicotine medicines and smokeless tobacco suggest that nicotine without burned tobacco smoke carries a low heart risk compared with smoking, but it is still a concern for people who already have heart disease. The authors report that e-cigarettes, which deliver nicotine without burning tobacco, appear to carry low heart risk in healthy users, at least with short-term use.

Benowitz NL, Burbank AD (2016). Cardiovascular toxicity of nicotine: Implications for electronic cigarette use. Trends Cardiovasc Med. — PubMed PMID: 27079891 · doi:10.1016/j.tcm.2016.03.001

Smokeless tobacco, sport and the heart

Review, 2015. This review looks at smokeless tobacco (snuff and chewing tobacco), which many young athletes use because nicotine can improve some aspects of performance. The authors report that nicotine raises heart rate, blood pressure and the heart's oxygen needs at rest and during moderate exercise. It also lowers heart rate variability, makes irregular heart rhythms more likely, harms the lining of blood vessels and may narrow the heart's arteries during and after exercise, while reducing muscle strength and short bursts of effort. Nicotine may reduce anxiety and improve concentration, agility, aerobic performance and weight control, but it is addictive, and the authors conclude that smokeless tobacco should be discouraged in sport and added to the World Anti-Doping Agency's list of banned substances.

Chagué F, Guenancia C, Gudjoncik A et al. (2015). Smokeless tobacco, sport and the heart. Arch Cardiovasc Dis. — PubMed PMID: 25497687 · doi:10.1016/j.acvd.2014.10.003

Nicotine exposure alters human vascular smooth muscle cell phenotype from a contractile to a synthetic type

Cell study, 2014. Researchers exposed human aorta smooth muscle cells grown in the lab to a small amount of nicotine for 48 hours to see whether nicotine itself changes how these artery-wall cells behave. After nicotine exposure, markers of the 'synthetic' cell type seen in artery plaques rose (one by 2.93-fold), while markers of the normal 'contractile' type fell (for example to 0.40-fold), and two cell-signaling enzymes became more active. The authors concluded that nicotine can shift these cells toward the plaque-associated type, likely through nicotinic acetylcholine receptors. This result is from cells in a dish only, not from people or animals.

Yoshiyama S, Chen Z, Okagaki T et al. (2014). Nicotine exposure alters human vascular smooth muscle cell phenotype from a contractile to a synthetic type. Atherosclerosis. — PubMed PMID: 25463075 · doi:10.1016/j.atherosclerosis.2014.10.019

NF-κB pathway mediates vascular smooth muscle response to nicotine

Cell study, 2013. Researchers studied how nicotine affects smooth muscle cells from blood vessel walls. They grew the cells in the lab, either alone or alongside the cells that line blood vessels. Nicotine switched on a signalling pathway called NF-κB, raised the levels of the cells' internal scaffolding proteins and made the cells move more. Blocking the α7 nicotinic receptor or the NF-κB pathway stopped these effects, and the authors conclude that contact signals between the two cell types help the muscle cells respond to nicotine; these results come from cells in a dish only.

Wang Z, Wu W, Tang M et al. (2013). NF-κB pathway mediates vascular smooth muscle response to nicotine. Int J Biochem Cell Biol. — PubMed PMID: 23142498 · doi:10.1016/j.biocel.2012.10.016

Nicotine-induced morphological changes in rat aorta: the protective role of melatonin

Animal study, 2012. Researchers gave rats nicotine by mouth for 28 days and looked at the main artery (the aorta) under the microscope, then gave some of the rats melatonin for another 28 days. After nicotine, three proteins linked to blood-vessel wall remodelling and clotting went up, very few cells were left in the artery's inner lining, and a new thickened inner layer (neointima) formed. In rats given melatonin after nicotine, the inner lining looked more like that of untreated rats and the thickened layer did not form. These results come from rats only, and the authors suggest melatonin could help keep blood-vessel walls healthy.

Rodella LF, Rossini C, Favero G et al. (2012). Nicotine-induced morphological changes in rat aorta: the protective role of melatonin. Cells Tissues Organs. — PubMed PMID: 21494021 · doi:10.1159/000324919

Nicotine aggravates the brain postischemic inflammatory response

Animal study, 2011. Researchers gave mice nicotine by injection for 14 days. Their blood nicotine levels reached about 100 ng/ml, which the authors say matches levels in average to heavy smokers. Then they studied what happened when blood flow to the brain was cut off and restored, which models a stroke. Compared with untreated mice, the nicotine-treated mice had more inflammatory signalling molecules in their small brain blood vessels and more white blood cells entering the brain, and they had larger areas of brain damage, worse neurological deficits and a higher death rate. These results come from mice only.

Bradford ST, Stamatovic SM, Dondeti RS et al. (2011). Nicotine aggravates the brain postischemic inflammatory response. Am J Physiol Heart Circ Physiol. — PubMed PMID: 21239632 · doi:10.1152/ajpheart.00928.2010

Cigarette smoking induces atrial fibrosis in humans via nicotine

Human observational study, 2007. Researchers compared heart tissue from 95 people having heart bypass surgery (46 smokers and 49 non-smokers) to see whether smoking is linked to scarring (fibrosis) in the upper chambers of the heart. In smokers, the amount of smoking over the years was the only factor linked to more scarring, and people who developed an irregular heartbeat (atrial fibrillation) after surgery had more scarring. When heart tissue from 8 non-smokers was exposed to nicotine in the laboratory, a scar-building collagen gene became up to 10 times more active, depending on the nicotine dose. The authors conclude that smoking contributes to this heart scarring through nicotine, and note that such scarring may make irregular heart rhythms more likely.

Goette A, Lendeckel U, Kuchenbecker A et al. (2007). Cigarette smoking induces atrial fibrosis in humans via nicotine. Heart. — PubMed PMID: 17395670 · doi:10.1136/hrt.2005.087171

Acute cardiovascular and sympathetic effects of nicotine replacement therapy

Human trial, 2006. In a randomized, blinded trial, 16 young healthy smokers (8 women) took a 4-mg nicotine tablet under the tongue or a placebo, and researchers measured heart rate, blood pressure, nerve signals that tighten blood vessels in the muscles, and breathing, both on room air and during 5 minutes of low oxygen. On room air, nicotine raised heart rate by 7 beats per minute, average blood pressure by 5 mm Hg and this nerve activity by 4 bursts per minute; during low oxygen it raised them by 8 beats per minute, 2 mm Hg and 7 bursts per minute. Nicotine also raised a marker of how much oxygen the heart uses, during normal breathing, low oxygen and breath-holds, while breathing, breath-hold length and blood oxygen levels did not change. The authors concluded that these effects did not come from a stronger reflex response to low oxygen, and that nicotine replacement raises the heart's oxygen use at times when less oxygen is available.

Najem B, Houssière A, Pathak A et al. (2006). Acute cardiovascular and sympathetic effects of nicotine replacement therapy. Hypertension. — PubMed PMID: 16651463 · doi:10.1161/01.HYP.0000219284.47970.34

Nicotine could augment adhesion molecule expression in human endothelial cells through macrophages secreting TNF-alpha, IL-1beta

Cell study, 2004. This laboratory study looked at how nicotine affects immune cells called macrophages and the cells that line blood vessels, using a macrophage cell line and human blood-vessel lining cells taken from umbilical cords. Macrophages treated with nicotine released more of two inflammatory signals, TNF-alpha and IL-1beta, which peaked at a nicotine concentration of 0.06 mM after 24 and 12 hours. Two other signals, IL-8 and IFN-gamma, did not change significantly. When the blood-vessel cells were exposed to fluid from these macrophages, they made more adhesion molecules and let more white blood cells stick to them, and blocking TNF-alpha and IL-1beta stopped this. The authors suggest this may be one way nicotine contributes to blood-vessel dysfunction, but the results come only from cells grown in a dish.

Wang Y, Wang L, Ai X et al. (2004). Nicotine could augment adhesion molecule expression in human endothelial cells through macrophages secreting TNF-alpha, IL-1beta. Int Immunopharmacol. — PubMed PMID: 15454119 · doi:10.1016/j.intimp.2004.07.028

Nicotine promotes arteriogenesis

Animal study, 2003. Researchers blocked the main leg artery in one leg of 85 rabbits and, for 21 days, delivered nicotine, a known blood-vessel growth factor (basic fibroblast growth factor), or an inactive solution directly into the artery through small implanted pumps. Nicotine increased the number of tiny blood vessels in the starved leg about as much as the growth factor did, and it also improved artery imaging scores, blood pressure in the calf, and blood flow. In lab tests, nicotine made white blood cells called monocytes stick to and cross the blood-vessel lining more readily, and raised several adhesion and signaling molecules two- to three-fold. The authors conclude that, in the short term, nicotine promotes the growth of new blood vessels and arteries in tissue with poor blood supply, but these results come only from rabbits and lab-grown cells, not from people.

Heeschen C, Weis M, Cooke JP (2003). Nicotine promotes arteriogenesis. J Am Coll Cardiol. — PubMed PMID: 12575981 · doi:10.1016/s0735-1097(02)02818-8

Smoking and ischemic stroke: a role for nicotine?

Review, 2002. This review looks at whether nicotine itself helps explain why cigarette smoking raises the risk of ischemic stroke, a question it describes as controversial. Nicotine taken through the skin or by mouth does not appear to carry as many health risks as cigarettes, but nicotine does act quickly on blood vessels and can stimulate the growth of cells in the vessel wall. The authors write that nicotine might change how the blood-brain barrier works and disturb the cells that line blood vessels. Some of these harmful effects are blocked by drugs that block nicotinic receptors, but newer studies suggest nicotine may also act through cell signals that do not involve these receptors, so the authors conclude that nicotine's effect on blood vessels in the brain should not be dismissed.

Hawkins BT, Brown RC, Davis TP (2002). Smoking and ischemic stroke: a role for nicotine?. Trends Pharmacol Sci. — PubMed PMID: 11830264 · doi:10.1016/s0165-6147(02)01893-x

Sympathectomy inhibits the vasoactive effects of nicotine in conscious rats

Animal study, 1999. This study in awake rats looked at how nicotine injected into a vein (1 to 100 micrograms per kilogram) raises blood pressure and heart rate. Nicotine raised both, and more so at higher doses. Both effects disappeared when the rats' sympathetic nerve endings were chemically destroyed. Blocking alpha-adrenergic receptors stopped the rise in blood pressure but not the faster heart rate, while blocking vasopressin receptors changed neither. The authors concluded that in rats nicotine raises blood pressure mainly by making blood vessels narrow through noradrenaline-like signals released from nerves rather than from the adrenal glands, and that vasopressin plays no significant role. These results are in animals only.

Marano G, Ramirez A, Mori I et al. (1999). Sympathectomy inhibits the vasoactive effects of nicotine in conscious rats. Cardiovasc Res. — PubMed PMID: 10435011 · doi:10.1016/s0008-6363(98)00326-5

The role of nicotine in smoking-related cardiovascular disease

Review, 1997. This is a review paper examining nicotine's possible role in cardiovascular disease linked to smoking. It concludes that nicotine activates the sympathetic nervous system and animal and mechanistic studies suggest it might speed up atherosclerosis, but human evidence is not strong enough to confirm this. The review states nicotine likely contributes to acute cardiovascular events through its effects on heart rate and blood pressure, though these effects are judged much less important than the clot-promoting effects of cigarette smoke or carbon monoxide. It also notes nicotine does not appear to increase blood clotting in humans, based on studies of pipe smokers and people using transdermal nicotine, and that the relationship between nicotine dose and cardiovascular risk appears flat.

Benowitz NL (1997). The role of nicotine in smoking-related cardiovascular disease. Prev Med. — PubMed PMID: 9245658 · doi:10.1006/pmed.1997.0175

Effect of nicotine on the intimal hyperplasia after endothelial removal of the rabbit carotid artery

Animal study, 1997. Rabbits had the lining of one artery (carotid) deliberately damaged and were then given oral nicotine for seven weeks, reaching blood nicotine levels similar to human smokers. Nicotine tended to speed up the abnormal thickening of the artery wall that follows this kind of injury, worsened the impairment in the artery's ability to relax (dilate) in response to certain chemical signals, increased two natural blockers of nitric oxide production in the regrown lining cells, and tended to raise levels of a blood-vessel-constricting substance (endothelin-1) in the thickened artery wall.

Hamasaki H, Sato J, Masuda H et al. (1997). Effect of nicotine on the intimal hyperplasia after endothelial removal of the rabbit carotid artery. Gen Pharmacol. — PubMed PMID: 9184797 · doi:10.1016/s0306-3623(96)00369-2

Nicotine and sympathetic neurotransmission

Review, 1997. This review explains how nicotine raises heart rate, the force of the heart's pumping and blood pressure. Nicotine switches on nicotinic receptors on nerve endings and in the adrenal glands, which release stress chemicals such as norepinephrine; the review describes step by step how the receptor opens to let sodium and calcium into the cell. In isolated guinea-pig hearts, and in human heart tissue studied in the laboratory, a heart starved of energy released more norepinephrine in response to nicotine. The authors report that this raises the heart's oxygen demand while narrowing its blood vessels, which is especially harmful in people with coronary artery disease and may trigger heart attacks or dangerous heart rhythms.

Haass M, Kübler W (1997). Nicotine and sympathetic neurotransmission. Cardiovasc Drugs Ther. — PubMed PMID: 9110108 · doi:10.1007/BF00053022

A clinical pharmacological study of subcutaneous nicotine

Human trial, 1993. Researchers gave 6 smokers a labeled form of nicotine by injection under the skin, at four different doses, and tracked blood levels for 8 hours. Peak blood nicotine levels rose in step with the dose, and the body absorbed essentially all of the injected nicotine. Heart rate rose more consistently with dose than blood pressure did, while people's subjective reactions varied widely from person to person. The paper concludes that this injection method is a practical and safe way to study nicotine's effects in people.

Le Houezec J, Jacob P, Benowitz NL (1993). A clinical pharmacological study of subcutaneous nicotine. Eur J Clin Pharmacol. — PubMed PMID: 8491235 · doi:10.1007/BF00271362

Performance, subjective, and physiological effects of nicotine in non-smokers

Human trial, 1993. Sixteen adults with little or no tobacco experience were given increasing doses of nicotine gum (0, 2, and 4 mg) during one session. Higher doses raised heart rate and blood pressure, lowered skin temperature, and were rated as stronger and more unpleasant with less desire to repeat. On cognitive tests, higher doses tended to lower accuracy and slow response time on three of four tasks, and the study concluded nicotine did not improve mental performance in these non-smokers.

Heishman SJ, Snyder FR, Henningfield JE (1993). Performance, subjective, and physiological effects of nicotine in non-smokers. Drug Alcohol Depend. — PubMed PMID: 8174498 · doi:10.1016/0376-8716(93)90041-n

Smoking and mechanisms of cardiovascular control

Review, 1988. This review looks at how nicotine affects the heart and blood vessels in people. It reports that a short dose of nicotine, whether from smoking or from an injection into a vein, typically raises blood pressure by 5 to 10 mm Hg and heart rate by 10 to 25 beats per minute, and that smoking weakens the heart's pumping in patients with angina or heart failure. The authors explain that nicotine acts in more ways than the classic nerve-relay explanation covers, including a strong blood-pressure-raising effect in an area of the brainstem. They note that little data exists on whether certain blood pressure medicines can prevent nicotine's short-term effects on the heart and blood vessels.

Robertson D, Tseng CJ, Appalsamy M (1988). Smoking and mechanisms of cardiovascular control. Am Heart J. — PubMed PMID: 3276114 · doi:10.1016/0002-8703(88)90646-1

The effect of nicotine on cultured cells of vascular origin

Cell study, 1985. Researchers exposed cells grown in the lab from blood vessels to nicotine at a range of concentrations. The cells were lining (endothelial) cells, smooth muscle cells and connective-tissue (fibroblast) cells, taken from healthy pigs, cattle or human fetal tissue. Nicotine increased the production and assembly of the cell's internal scaffolding proteins (the cytoskeleton). The effect was clearest in smooth muscle cells and partly seen in lining cells, while fibroblasts showed no change at the doses tested. These results come only from cells in a dish, not from animals or people.

Csonka E, Somogyi A, Augustin J et al. (1985). The effect of nicotine on cultured cells of vascular origin. Virchows Arch A Pathol Anat Histopathol. — PubMed PMID: 3931344 · doi:10.1007/BF00709990

Transdermal administration of nicotine

Human trial, 1984. One adult man had nicotine applied to the skin of his forearm in a liquid solution, and researchers tracked nicotine levels in his saliva plus his heart rate and blood pressure for 12 hours afterward. Within 30 minutes his saliva showed a nicotine level of 50 ng/ml, his pulse rose by 15 beats per minute, and his systolic blood pressure rose by 10 mmHg; nicotine levels stayed elevated for 2 hours and were similar to levels seen from cigarette smoking. The researchers suggested that this skin-based method of giving nicotine might be worth studying as a way to help people cut back or quit smoking.

Rose JE, Jarvik ME, Rose KD (1984). Transdermal administration of nicotine. Drug Alcohol Depend. — PubMed PMID: 6734425 · doi:10.1016/0376-8716(84)90061-9

Acute microcirculatory response to nicotine in frog web

Animal study, 1982. This study tested how nicotine affects tiny blood vessels in frog webbed feet. Researchers soaked the web in a nicotine solution for 4 minutes and measured blood flow speed and vessel diameter. Blood flow and vessel widening (vasodilation) increased after nicotine exposure, and this effect lasted even after the heart's pumping pressure returned to normal, suggesting nicotine itself was absorbed through the tissue and caused the blood vessels to widen.

Horimoto M, Koyama T (1982). Acute microcirculatory response to nicotine in frog web. Jpn J Physiol. — PubMed PMID: 7154432 · doi:10.2170/jjphysiol.32.771

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PubMed Topic Searches

1. PubMed: Heart and Blood Vessels and nicotine (the search this page is built from)

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Connections

• How Your Body Controls Blood Pressure — interactive animation
• Nicotine: The Research
• The Nicotine Patch, animated
• Nicotinic Acetylcholine Receptors
• Cigarette Smoke — what burnt tobacco adds that nicotine alone does not
• Brain and Memory
• Mood and Mental Health
• Inflammation and Immunity
• Cancer Research
• Metabolism and Weight
• Addiction and Withdrawal
• Patches, Gum and Delivery
• Toxicity and Safety

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