Nicotine and heart rate

Does Nicotine Raise Heart Rate? What Measurement Can Show

Yes. Nicotine raises heart rate shortly after intake, and the racing pulse belongs to the molecule rather than the smoke, so local delivery does not contain it. Heart rate variability, autonomic reflex testing and arterial stiffness measurement show how your own pulse and vessels respond.

A cholinergic drug does not stay where you put it. If you have read that nicotine calms a colitis flare or moves a stalled bowel, the numbers worth having first are your own pulse, vessels and blood work.

Does nicotine raise heart rate? In people using electronic nicotine delivery devices, the National Academies of Sciences, Engineering, and Medicine graded the evidence as substantial that heart rate climbs shortly after intake. Asked whether those same devices cause clinical cardiovascular events, the committee wrote that no evidence is available either way, which is a statement of ignorance and not a safety claim. The video above, the last one in The Angry Gut by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes, is about where a drug is placed, not whether anyone should take it. The question here is narrower: if a cholinergic drug is moving through you for any reason, which of your own numbers move with it, and who is watching them?

Why a gut question becomes a heart question

The nervous system in your gut wall is the first brain, and the organ in your skull is the second one, sitting downstream. That first brain runs substantially on acetylcholine, and nicotine imitates acetylcholine well enough to be heard at two separate addresses. One is on the nerve cells of the bowel wall, where the signal drives contraction. The other is a receptor called alpha-7, on immune cells, where acetylcholine turns down release of TNF, one of the loudest inflammatory alarms the body has. That immune requirement was established in mice bred without alpha-7, in which the vagal quieting of TNF disappears. Mouse work, and it reads as mouse work.

Neither address is reachable except through the bloodstream that also supplies your heart and your arteries. So a racing pulse and a spike in blood pressure belong to the molecule rather than to the smoke, and local delivery is not the same thing as contained delivery. Given rectally, the drug peaked in blood 44 to 50 minutes afterward and rose with the dose, and 11 of 14 recorded adverse events fell in the window from 30 to 105 minutes, most at the highest dose studied.

Does nicotine raise heart rate? The one trial that asked never printed a pulse

Forty-five nonsmokers whose ulcerative colitis was quiet were randomized, double-blind, to a nicotine patch or a placebo patch for twelve weeks, with twenty of them getting the drug. The investigators measured platelet volume and a platelet surface marker, a circulating marker of damage to the vessel lining, plasma fibrinogen, white cell count and serum lipids. Fibrinogen fell. Platelet activation, the vessel-lining marker, the white cell count and the lipids did not budge.

Now notice what is missing. Fibrinogen rises with inflammation anywhere, so in an inflamed bowel a falling fibrinogen may be reporting on the colon rather than on the arteries. Twenty exposed patients over twelve weeks cannot establish cardiovascular safety for anybody. And the report carries no blood pressure and no heart rate, the two numbers a patient actually asks about. Across this literature, what was convenient to assay got assayed, and what the person wanted to know was left out.

What can be measured, and what is done elsewhere

Measura [Cardiometabolic and Autonomic Health Analysis] does not look inside your colon. Endoscopy, stool studies and motility studies are gastroenterology tests done in other settings, and those are the tests that describe bowel disease itself. Measura measures; it does not treat, and it does not diagnose on its own. Findings go to the physician who cares for you.

What can be put on a chart is the rest of the body a drug travels through. Heart rate variability records the beat-to-beat variation in the gap between heartbeats. Autonomic nervous system testing and cardiac autonomic reflex tests record how your heart rate and blood pressure answer standard challenges such as standing up and paced breathing. Arterial stiffness and endothelial function testing looks at the large vessels and at how a vessel lining behaves, which is the thing that old patch trial could only approach through a blood marker. Laboratory panels carry the blood work your physician selects, and what a variability number actually means is worth reading before you have one done.

There is a reason to trust your own response over a drug level. Among twenty healthy volunteers given nicotine by mouth and by vein, the serum concentration did not predict who felt unwell. In a rectal pilot, 4 of 10 patients had side effects while their serum nicotine sat low or undetectable. A level describes the drug. Measurement describes you.

Two drivers in the body, one in the market

The biology has two arms that do not point the same way. Cholinergic signaling in the gut wall moves the bowel and quiets the immune cells embedded in it, so withdrawing a twenty-year cholinergic input from a lining that had adapted to it is a physiological event with a named receptor behind it, not a coincidence of timing. The second arm is the autonomic and vascular response to that same alkaloid arriving everywhere at once, layered on whatever metaflammation, the low-grade inflammation that keeps a metabolism irritated, is already running. The third driver is not biology: nobody owns an off-patent molecule, so nobody funds the trial that would settle it, and the dependence does not leave when the smoke does.

There is nothing to buy and nothing to improvise

The book argues about a route: a small dose held against the lining of the lower colon, not a patch on an arm. When a liquid version of that route was randomized, remission reached 27% on nicotine against 33% on placebo. A suppository, meanwhile, has never been given to a human being for anything. One group built such formulations, measured how they let the drug go in a dish, and stopped there. That is an absence of evidence rather than a negative result, and an absence licenses a study, not a prescription.

Two more things are worth keeping straight. Nobody has ever measured how much nicotine reaches rectal tissue, so the local-dose idea rests on blood drawn a compartment away. And on movement, one claim holds and one does not. High-amplitude propagated contractions did appear in healthy subjects after a large dose, with faster transit: mass peristalsis, the wave that empties a colon. No controlled human trial supports using the drug to restart the fasting housekeeping sweep of the stomach and small bowel.

Judging a compound by its reputation instead of its biochemistry is not caution.

Neither is improvising. Nothing is sold for this purpose, no dose has been established outside a trial protocol, and there is no reason for anyone to take up nicotine in any form. Do not start, stop or change a medication because of something you read; that sits with your prescriber. Rescue is not repair, and the first brain answers to being fed and tended long before it answers to an alkaloid.

What to ask before anything changes

• When symptoms began relative to the day you quit, in months or in years.
• Where your disease sits, since every promising signal here lives in the left colon.
• What has already been tried, and whether anything remains in the standard sequence.
• If nicotine is ever offered in any form, the plan for your heart rate and blood pressure, and how long the trial runs before somebody calls it.

More prompts sit in questions worth asking your doctor. Every study behind these figures, with its limits beside it, is in the companion deep dive, and the clinician version is the screening discussion for practices.

Frequently asked questions

References

• National Academies of Sciences, Engineering, and Medicine, Health and Medicine Division, Board on Population Health and Public Health Practice, & Committee on the Review of the Health Effects of Electronic Nicotine Delivery Systems. (2018). Public health consequences of e-cigarettes. National Academies Press (consensus study report), Consensus study report, chapter conclusions. https://pubmed.ncbi.nlm.nih.gov/29894118/
• Wang, H., Yu, M., Ochani, M., Amella, C. A., Tanovic, M., Susarla, S., Li, J. H., Wang, H., Yang, H., Ulloa, L., Al-Abed, Y., Czura, C. J., & Tracey, K. J. (2003). Nicotinic acetylcholine receptor alpha7 subunit is an essential regulator of inflammation. Nature, 421(6921), 384-388. https://doi.org/10.1038/nature01339
• Thomas, G. A., Davies, S. V., Rhodes, J., Russell, M. A., Feyerabend, C., & Säwe, U. (1995a). Is transdermal nicotine associated with cardiovascular risk? Journal of the Royal College of Physicians of London, 29(5), 392-396. https://pubmed.ncbi.nlm.nih.gov/8847680/
• Ingram, J. R., Routledge, P., Rhodes, J., Marshall, R. W., Buss, D. C., Evans, B. K., Feyerabend, C., & Thomas, G. A. O. (2004). Nicotine enemas for treatment of ulcerative colitis: A study of the pharmacokinetics and adverse events associated with three doses of nicotine. Alimentary Pharmacology & Therapeutics, 20(8), 859-65. https://doi.org/10.1111/j.1365-2036.2004.02199.x
• Ingram, J. R., Thomas, G. A. O., Rhodes, J., Green, J. T., Hawkes, N. D., Swift, J. L., Srivastava, E. D., Evans, B. K., Williams, G. T., Newcombe, R. G., Courtney, E., & Pillai, S. (2005). A randomized trial of nicotine enemas for active ulcerative colitis. Clinical Gastroenterology and Hepatology, 3(11), 1107-1114. https://doi.org/10.1016/s1542-3565(05)00849-9
• Sandborn, W. J., Tremaine, W. J., Leighton, J. A., Lawson, G. M., Zins, B. J., Compton, R. F., Mays, D. C., Lipsky, J. J., Batts, K. P., Offord, K. P., Hurt, R. D., & Green, J. (1997). Nicotine tartrate liquid enemas for mildly to moderately active left-sided ulcerative colitis unresponsive to first-line therapy: A pilot study. Alimentary Pharmacology & Therapeutics, 11(4), 663-71. https://doi.org/10.1046/j.1365-2036.1997.00208.x
• Compton, R. F., Sandborn, W. J., Lawson, G. M., Sheets, A. J., Mays, D. C., Zins, B. J., Tremaine, W. J., Lipsky, J. J., Mahoney, D. W., Zinsmeister, A. R., Offord, K. P., Hurt, R. D., Evans, B. K., & Green, J. (1997). A dose-ranging pharmacokinetic study of nicotine tartrate following single-dose delayed-release oral and intravenous administration. Alimentary Pharmacology & Therapeutics, 11(5), 865-74. https://doi.org/10.1046/j.1365-2036.1997.00236.x
• Coulie, B., Camilleri, M., Bharucha, A. E., Sandborn, W. J., & Burton, D. (2001). Colonic motility in chronic ulcerative proctosigmoiditis and the effects of nicotine on colonic motility in patients and healthy subjects. Alimentary Pharmacology & Therapeutics, 15(5), 653-663. https://doi.org/10.1046/j.1365-2036.2001.00959.x
• Dash, A. K., Gong, Z., Miller, D. W., Huai-Yan, H., & Laforet, J. (1999). Development of a rectal nicotine delivery system for the treatment of ulcerative colitis. International Journal of Pharmaceutics, 190(1), 21-34. https://doi.org/10.1016/s0378-5173(99)00221-5
• Pandolfino, J. E., & Kahrilas, P. J. (2000). Smoking and gastro-oesophageal reflux disease. European Journal of Gastroenterology & Hepatology, 12(8), 837-842. https://doi.org/10.1097/00042737-200012080-00002

Related reading

• How to Test for MCAS When Your Allergy Tests Keep Coming Back Negative
• Heart Rate Variability

Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP, medical director of Measura. Last reviewed September 12, 2026.