Evidence suggests that β-Adrenergic receptor signaling increases heart rate and force through not just cyclic AMP but also the Ca(2+)-releasing second messengers NAADP (nicotinic acid adenine dinucleotide phosphate) and cADPR (cyclic ADP-ribose). Nevertheless, proof of the physiological relevance of these messengers requires direct measurements of their levels in response to receptor stimulation. Here we report that in intact Langendorff-perfused hearts β-adrenergic stimulation increased both messengers, with NAADP being transient and cADPR being sustained. Both NAADP and cADPR have physiological and therefore pathological relevance by providing alternative drug targets in the β-adrenergic receptor signaling pathway.

Original publication

DOI

10.1016/j.bbrc.2012.09.054

Type

Journal

Biochem Biophys Res Commun

Publication Date

19/10/2012

Volume

427

Pages

326 - 329

Keywords

Adrenergic beta-Agonists, Animals, Cyclic ADP-Ribose, Guinea Pigs, Heart, In Vitro Techniques, Myocardium, NADP, Receptors, Adrenergic, beta, Signal Transduction