Adrenoceptor sub-type involvement in Ca2+ current stimulation by noradrenaline in human and rabbit atrial myocytes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2022-09-22

AUTHORS

Priyanka Saxena, Rachel C. Myles, Godfrey L. Smith, Antony J. Workman

ABSTRACT

Atrial fibrillation (AF) from elevated adrenergic activity may involve increased atrial L-type Ca2+ current (ICaL) by noradrenaline (NA). However, the contribution of the adrenoceptor (AR) sub-types to such ICaL-increase is poorly understood, particularly in human. We therefore investigated effects of various broad-action and sub-type-specific α- and β-AR antagonists on NA-stimulated atrial ICaL. ICaL was recorded by whole-cell-patch clamp at 37 °C in myocytes isolated enzymatically from atrial tissues from consenting patients undergoing elective cardiac surgery and from rabbits. NA markedly increased human atrial ICaL, maximally by ~ 2.5-fold, with EC75 310 nM. Propranolol (β1 + β2-AR antagonist, 0.2 microM) substantially decreased NA (310 nM)-stimulated ICaL, in human and rabbit. Phentolamine (α1 + α2-AR antagonist, 1 microM) also decreased NA-stimulated ICaL. CGP20712A (β1-AR antagonist, 0.3 microM) and prazosin (α1-AR antagonist, 0.5 microM) each decreased NA-stimulated ICaL in both species. ICI118551 (β2-AR antagonist, 0.1 microM), in the presence of NA + CGP20712A, had no significant effect on ICaL in human atrial myocytes, but increased it in rabbit. Yohimbine (α2-AR antagonist, 10 microM), with NA + prazosin, had no significant effect on human or rabbit ICaL. Stimulation of atrial ICaL by NA is mediated, based on AR sub-type antagonist responses, mainly by activating β1- and α1-ARs in both human and rabbit, with a β2-inhibitory contribution evident in rabbit, and negligible α2 involvement in either species. This improved understanding of AR sub-type contributions to noradrenergic activation of atrial ICaL could help inform future potential optimisation of pharmacological AR-antagonism strategies for inhibiting adrenergic AF. More... »

PAGES

1311-1321

References to SciGraph publications

  • 1994-06. Adrenergic modulation of potassium currents in isolated human atrial myocytes in JOURNAL OF BIOMEDICAL SCIENCE
  • 2011-12-08. Remodelling of human atrial K+ currents but not ion channel expression by chronic β-blockade in PFLÜGERS ARCHIV - EUROPEAN JOURNAL OF PHYSIOLOGY
  • 2009-12-04. Cardiac adrenergic control and atrial fibrillation in NAUNYN-SCHMIEDEBERG'S ARCHIVES OF PHARMACOLOGY
  • 1985-10. The affinity of (−)-propranolol for β1- and β1-autoreceptors of human heart in NAUNYN-SCHMIEDEBERG'S ARCHIVES OF PHARMACOLOGY
  • 1992-07. Electrophysiologic and inotropic effects of α-adrenoceptor stimulation in human isolated atrial heart muscle in NAUNYN-SCHMIEDEBERG'S ARCHIVES OF PHARMACOLOGY
  • 1992-07. Modulation of cytosolic free calcium concentration by α1-adrenoceptors in rat atrial cells in NAUNYN-SCHMIEDEBERG'S ARCHIVES OF PHARMACOLOGY
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    URI

    http://scigraph.springernature.com/pub.10.1007/s00424-022-02746-z

    DOI

    http://dx.doi.org/10.1007/s00424-022-02746-z

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1151190257

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/36131146


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