Evidence map›Paper›PMID 23333294›Full record

ArticleDrug and alcohol dependence2013

Patterns of nicotinic receptor antagonism II: cardiovascular effects in rats.

Emily M Jutkiewicz, Kenner C Rice, F Ivy Carroll, James H Woods

Abstract read
In one paragraph

Article in Drug and alcohol dependence, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Copper-Mediated Homocoupling ofMolecules (Basel, Switzerland) · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Novel Antimuscarinic Antidepressant-like Compounds with Reduced Effects on Cognition.The Journal of pharmacology and experimental therapeutics · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Evaluation of the cardiovascular effects of varenicline in rats.Drug design, development and therapy · 2015
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Emily M JutkiewiczDepartment of Pharmacology, University of Michigan, 1150 W Medical Center Drive, Ann Arbor, MI 48109-5632, USA.
Kenner C Rice
F Ivy Carroll
James H Woods
University of Michigan–Ann Arbor · USNational Institute on Alcohol Abuse and Alcoholism · USRTI International · US

Funding

POSTDOCTORAL TRAINING IN THE BIOLOGY OF DRUG ABUSET32DA007268 · NIDA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI TRAYNOR, JOHN R. · 1991 to 2021
$6.7M
Medicinal Chemistry of Drugs Acting on Biogenic Amine ReceptorsZIADA000532 · NIDA · NATIONAL INSTITUTE ON DRUG ABUSE · PI RICE, KENNER · 2009 to 2020
$4.5M
Intramural NIH HHSNIDA NIH HHS T32 DA007268
6 · The paper itself

Abstract

backgroundTobacco cessation pharmacotherapies currently are limited to nicotine itself, the partial nicotine agonists varenicline and cytisine, and the antidepressant bupropion. Compared with agonists, nicotinic antagonists such as the noncompetitive, nonselective compound mecamylamine, and the competitive, α4β2-preferring antagonist dihydro-β-erythroidine (DHβE) may be a novel approach to the treatment of tobacco smoking as both are effective antagonists of nicotine's central effects. Considering nicotinic acetylcholine receptors mediate critical peripheral effects of acetylcholine, such as cardiovascular effects, it is important to study how nicotinic antagonists would alter the cardiovascular system and the cardiovascular changes induced by nicotine.

methodsThe effects of several nicotinic agonists and antagonists on blood pressure and heart rate were measured in conscious, unrestrained rats following parenteral administration using a telemetry system.

resultsNicotine and other nicotinic receptor agonists (epibatidine, varenicline, and cytisine) produced similar increases in blood pressure, whereas their effects on heart rate were biphasic. The cardiovascular changes were attenuated by the nonselective nicotine antagonist, mecamylamine, but the peripherally restricted antagonist hexamethonium blocked only the agonist-induced changes in blood pressure. The α7-preferring antagonist, MLA, and the α4β2-preferring antagonist, DHβE, were much less effective in blocking the agonist-induced cardiovascular changes, indicating that nicotine's cardiovascular effects, are due to activation at autonomic ganglia involving nicotinic receptor subtypes other than α4, α7, or β2.

conclusionsThe data indicate that the cardiovascular effects of nicotine and nicotine-like agents are mediated through receptor mechanisms that are distinct from those that mediate the central effects of nicotine.

Indexed as

AnimalsBlood PressureDose-Response Relationship, DrugHeart RateMaleNicotinic AntagonistsRatsRats, Sprague-DawleyReceptors, NicotinicNicotinic Antagonistsnicotinic receptor alpha4beta2Receptors, NicotinicCardiovascular effectsNicotineNicotinic agonistsRats

Identifiers

PMID23333294
PMCPMC4174279
OpenAlexW1965391128

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.