ArticleFrontiers in physiology2026
Extended secondhand smoke exposure alters potassium channel activity and reduces excitability of cardiac vagal neurons in mice.
Article in Frontiers in physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Background: Despite the decline in secondhand smoke (SHS) exposure since the implementation of smoking bans in public places, SHS exposure remains a significant health risk factor affecting about 1/3 of non-smokers worldwide. We previously showed that 12 weeks of SHS exposure reduces heart rate variability, an effect that peaks at week 4. We further showed that 4 weeks of SHS exposure significantly reduces cardiac vagal neuron's (CVN) excitability that is associated with a reduced small conductance calcium-dependent potassium (SK) channel activity. Objectives: This study aimed to test whether the reduced excitability in CVNs also wanes with longer exposure duration (12 weeks) and whether 4-aminopyridine sensitive voltage-gated potassium channels contribute to the SHS-induced decreases in neuronal excitability. Methods: Adult male mice were exposed to 12 weeks of filtered air or SHS at an environmental-relevant concentration (3 mg/m Results: 12 weeks of SHS exposure significantly increased action potential (AP) thresholds and reduced spiking responses to excitation. SHS exposure did not significantly alter resting membrane potential, or 4-aminopyridine sensitive channel activity, suggesting that leak potassium channels and voltage gated potassium channels were unlikely to contribute to the reduced excitability. We found two adaptations that may serve to counteract the reduced excitability. First, APs inactivated at higher voltages that helped to maintain the spiking response range and increase maximum discharge frequency. Second, blocking SK channels with apamin had smaller effects on the spiking response in CVNs from SHS-exposed mice, suggesting that a reduced SK channel activation during spiking activity may help to dampen the reduced excitability. Conclusion: Environmentally relevant SHS exposure reduces neuronal excitability of CVNs through mechanisms other than enhanced SK and voltage-gated potassium channel functions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.