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Methods for the Isolation, Culture, and Functional Characterization of Sinoatrial Node Myocytes from Adult Mice

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Published on: October 23, 2016

Depressed HCN4 function in the type 2 diabetic sinoatrial node.

Sajida Parveen¹, Paddy H S Cheah¹, Luke P I Worthington¹

¹Department of Physiology, School of Biomedical Sciences, and HeartOtago, University of Otago, Dunedin, Otago, New Zealand.

Molecular and Cellular Biochemistry

|December 27, 2022

Summary

Type 2 diabetes impairs heart rate control by reducing HCN4 channel expression and function in the sinoatrial node. This study reveals key mechanisms behind diabetic bradycardia.

Keywords:

Heart rate Sinoatrial node Type 2 diabetes

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Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice

Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice

Published on: July 5, 2021

Area of Science:

Cardiovascular Physiology
Diabetology
Molecular Cardiology

Background:

Type 2 diabetes mellitus (T2DM) is associated with impaired autonomic control of heart rate (HR).
Intrinsic HR generation within the sinoatrial node (SAN) may be affected in T2DM, as suggested by previous findings of lower ex vivo HR in diabetic rat hearts.
Hyperpolarisation-activated cyclic nucleotide-gated 4 (HCN4) channels are critical for pacemaking in the SAN.

Purpose of the Study:

To investigate if reduced intrinsic HR in type 2 diabetic hearts is caused by alterations in HCN4 channel function, protein expression, or distribution.
To elucidate the molecular mechanisms underlying impaired cardiac chronotropy in T2DM.

Main Methods:

Isolated Langendorff-perfused hearts from Zucker type 2 Diabetic Fatty (ZDF) rats (DM) and non-diabetic littermates (nDM) were used.
Intrinsic HR response to HCN4 channel blockade with ivabradine was assessed.
HCN4 protein expression and membrane localization in the SAN were analyzed using western blot and immunofluorescence.

Main Results:

Intrinsic HR was significantly lower in DM hearts compared to nDM hearts.
The response to ivabradine was diminished in DM hearts, normalizing HR between groups.
HCN4 protein expression was decreased in the SAN of DM rats, with no change in membrane localization.

Conclusions:

Lower intrinsic HR in type 2 diabetic hearts is likely due to decreased HCN4 expression and impaired HCN4 channel function.
This study provides novel insights into the intrinsic mechanisms of altered HR regulation in T2DM.
Findings highlight HCN4 channels as a potential therapeutic target for diabetic cardiac dysfunction.