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Updated: Jun 25, 2025

Spectral Confocal Imaging of Fluorescently tagged Nicotinic Receptors in Knock-in Mice with Chronic Nicotine Administration
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Spectral Confocal Imaging of Fluorescently tagged Nicotinic Receptors in Knock-in Mice with Chronic Nicotine Administration

Published on: February 10, 2012

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Nicotine Impairs Smooth Muscle cAMP Signaling and Vascular Reactivity

Navid Singhrao1, Victor A Flores-Tamez1, Yumna A Moustafa1

  • 1Department of Pharmacology, University of California, Davis, California, USA.

Microcirculation (New York, N.Y. : 1994)
|May 28, 2024
PubMed
Abstract

Insights

Nicotine exposure reduces cyclic adenosine monophosphate (cAMP) production in vascular smooth muscle (VSM), impairing blood vessel relaxation. This effect, linked to nicotine products, may contribute to vascular complications.

Area of Science:

  • Cardiovascular Biology
  • Pharmacology
  • Molecular Signaling

Background:

  • Nicotine is a primary component of tobacco products and is known to affect cardiovascular health.
  • Vascular smooth muscle (VSM) plays a critical role in regulating blood pressure and vascular tone.
  • Cyclic adenosine monophosphate (cAMP) is a key second messenger involved in VSM relaxation and β-adrenergic signaling.

Purpose of the Study:

  • To investigate the impact of nicotine on receptor-mediated cAMP synthesis in VSM.
  • To determine if nicotine impairs β-adrenergic-mediated cAMP signaling in VSM.
  • To understand how nicotine affects vascular reactivity through alterations in cAMP signaling.

Main Methods:

  • Utilized VSM cells and acutely isolated aortas from mice engineered to express the cAMP sensor TEpacVV (Camper) specifically in VSM (CamperSM).
  • Assessed isoproterenol (ISO)-induced cAMP production in response to nicotine exposure and second-hand smoke (SHS).
  • Evaluated the functional consequences on ISO-induced vasodilation and the effect of phosphodiesterase 3 (PDE3) inhibition.

Main Results:

  • Nicotine significantly reduced ISO-induced cAMP production in VSM cells and arteries, confirmed using CamperSM mice.
  • Impaired cAMP signaling by nicotine hindered ISO-induced vasodilation.
  • Co-administration with a PDE3 inhibitor reversed the nicotine-induced impairment of vasodilation.

Conclusions:

  • Nicotine disrupts β-adrenergic-mediated cAMP signaling in VSM.
  • These alterations in cAMP signaling contribute to impaired vasodilation and may lead to vascular complications.
  • Findings highlight a potential mechanism linking nicotine use to cardiovascular disease risk.
Keywords:
biosensorse‐cigaretteshypertensionphosphodiesterasessecond‐hand smokewire myography

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