Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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 article

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