These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Neurohormonal Regulation of IKs in Heart Failure: Implications for Ventricular Arrhythmogenesis and Sudden Cardiac Death.
    Author: Shugg T, Hudmon A, Overholser BR.
    Journal: J Am Heart Assoc; 2020 Sep 15; 9(18):e016900. PubMed ID: 32865116.
    Abstract:
    Heart failure (HF) results in sustained alterations in neurohormonal signaling, including enhanced signaling through the sympathetic nervous system and renin-angiotensin-aldosterone system pathways. While enhanced sympathetic nervous system and renin-angiotensin-aldosterone system activity initially help compensate for the failing myocardium, sustained signaling through these pathways ultimately contributes to HF pathophysiology. HF remains a leading cause of mortality, with arrhythmogenic sudden cardiac death comprising a common mechanism of HF-related death. The propensity for arrhythmia development in HF occurs secondary to cardiac electrical remodeling that involves pathological regulation of ventricular ion channels, including the slow component of the delayed rectifier potassium current, that contribute to action potential duration prolongation. To elucidate a mechanistic explanation for how HF-mediated electrical remodeling predisposes to arrhythmia development, a multitude of investigations have investigated the specific regulatory effects of HF-associated stimuli, including enhanced sympathetic nervous system and renin-angiotensin-aldosterone system signaling, on the slow component of the delayed rectifier potassium current. The objective of this review is to summarize the current knowledge related to the regulation of the slow component of the delayed rectifier potassium current in response to HF-associated stimuli, including the intracellular pathways involved and the specific regulatory mechanisms.
    [Abstract] [Full Text] [Related] [New Search]