Universität zu Köln

Tevoufouet, Etienne E., Nembo, Erastus N., Distler, Fabian, Neumaier, Felix ORCID: 0000-0002-6376-6391, Hescheler, Jurgen, Nguemo, Filomain and Schneider, Toni (2017). Multiple nickel-sensitive targets elicit cardiac arrhythmia in isolated mouse hearts after pituitary adenylate cyclase-activating polypeptide-mediated chronotropy. Pharmacol. Res., 117. S. 140 - 148. LONDON: ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD. ISSN 1043-6618

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Abstract

The pituitary adenylate cyclase-activating polypeptide (PACAP)-27 modulates various biological processes, from the cellular level to function specification. However, the cardiac actions of this neuropeptide are still under intense studies. Using control (+I+) and mice lacking (-1-) either R-type (Ca(v)2.3) or T-type (Ca(v)3.2) Ca2(+) channels, we investigated the effects of PACAP-27 on cardiac activity of spontaneously beating isolated perfused hearts. Superfusion of PACAP-27 (20 nM) caused a significant increase of baseline heart frequency in Cav2.3(+1+) (156.9 10.8 to 239.4 23.4 bpm; p < 0.01) and Cav2.3(-1-) (190.3 +/- 26.4 to 270.5 +/- 25.8 bpm; p < 0.05) hearts. For Cav3.2, the heart rate was significantly increased in Cav3.2(-l-) (133.1 +/- 8.5 bpm to 204.6 +/- 27.9 bpm; p <0.05) compared to Cav3.2(+I+) hearts (185.7 +/- 11.2 bpm to 209.3 +/- 22.7 bpm). While the P wave duration and QTc interval were significantly increased in Cav2.3(+1+) and Cav2.3(-I-) hearts following PACAP-27 superfusion, there was no effect in Cav3.2(+I+) and Cav3.2(-l-) hearts. The positive chronotropic effects observed in the four study groups, as well as the effect on P wave duration and QTc interval were abolished in the presence of Ni2+ (50,mu M) and PACAP-27 (20 nM) in hearts from Cav2.3(+I+) and Cav2.3(-I-) mice. In addition to suppressing PACAP's response, Ni2+ also induced conduction disturbances in investigated hearts. In conclusion, the most Ni2+-sensitive Ca2+ channels (R-and T-type) may modulate the PACAP signaling cascade during cardiac excitation in isolated mouse hearts, albeit to a lesser extent than other Ni2+-sensitive targets. (C) 2016 Published by Elsevier Ltd.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Tevoufouet, Etienne E. UNSPECIFIED UNSPECIFIED UNSPECIFIED Nembo, Erastus N. UNSPECIFIED UNSPECIFIED UNSPECIFIED Distler, Fabian UNSPECIFIED UNSPECIFIED UNSPECIFIED Neumaier, Felix UNSPECIFIED orcid.org/0000-0002-6376-6391 UNSPECIFIED Hescheler, Jurgen UNSPECIFIED UNSPECIFIED UNSPECIFIED Nguemo, Filomain UNSPECIFIED UNSPECIFIED UNSPECIFIED Schneider, Toni UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-238326
DOI:	10.1016/j.phrs.2016.12.025
Journal or Publication Title:	Pharmacol. Res.
Volume:	117
Page Range:	S. 140 - 148
Date:	2017
Publisher:	ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
Place of Publication:	LONDON
ISSN:	1043-6618
Language:	English
Faculty:	Faculty of Mathematics and Natural Sciences
Divisions:	Faculty of Medicine > Physiologie und Pathophysiologie > Institut für Neurophysiologie
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language FUNCTIONAL EXPRESSION; POTENT VASODILATOR; CALCIUM-CHANNELS; CA2+ CHANNELS; RECEPTORS; PACAP; NEURONS; INFLUX; BLOCK; LOOP Multiple languages Pharmacology & Pharmacy Multiple languages
Refereed:	Yes
URI:	http://kups.ub.uni-koeln.de/id/eprint/23832