Send to

Choose Destination
See comment in PubMed Commons below
Fukushima J Med Sci. 2012;58(2):144-50.

Inhibitory effect of β-hydroxybutyric acid on L-type Ca(2+) current under β-adrenergic stimulation in guinea pig cardiac ventricular myocytes.

Author information

Department of Pharmacology, Faculty of Medicine, Fukushima Medical University, Fukushima, Japan.


Severe ketoacidosis induces heart failure and cardiac arrest, but its mechanism is unknown. Recently, hydroxy-carboxylic acid receptor 2 (HCA(2)) was found to be a receptor for a ketone body, β-hydroxybutyric acid (BHB), and is coupled with Gi-GTP binding protein. HCA(2) expression was reported in the guinea pig heart. Therefore, using guinea pig cardiac myocytes, we investigated effects of BHB on L-type Ca(2+) current pre-augmented with β-adrenoceptor agonist, isoproterenol under the whole-cell voltage clamp. BHB significantly reduced the Ca(2+) current pre-augmented with isoproterenol. The effect of BHB was concentration dependent with IC(50) of 1.1 mM. Nicotinic acid (NA), another ligand for HCA(2), also exerted an effect on the Ca(2+) current similar to that of BHB. The effects of BHB and NA were reduced by a specific Gi inhibitor, pertussis toxin in the pipette solution. Our results suggest that BHB activates Gi-coupled signal transduction pathway via HCA(2) in guinea pig cardiac myocytes. The HCA(2)-mediated signal transduction may be associated with ketoacidosis-induced cardiac suppression.

[Indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for J-STAGE, Japan Science and Technology Information Aggregator, Electronic
    Loading ...
    Support Center