Horm Metab Res 2016; 48(07): 476-483
DOI: 10.1055/s-0042-101794
Endocrine Research
© Georg Thieme Verlag KG Stuttgart · New York

Vasodilator Effect of Glucagon: Receptorial Crosstalk Among Glucagon, GLP-1, and Receptor for Glucagon and GLP-1

E. Sélley
1   2nd Department of Medicine and Nephrological Center University of Pécs, Pécs, Hungary
,
S. Kun
1   2nd Department of Medicine and Nephrological Center University of Pécs, Pécs, Hungary
,
I. A. Szijártó
2   Medical Clinic for Nephrology and Internal Intensive Care, Charité Campus Virchow Klinikum and Experimental and Clinical Research Center (ECRC), Max Delbrück Center for Molecular Medicine, Berlin, Germany
,
M. Kertész
1   2nd Department of Medicine and Nephrological Center University of Pécs, Pécs, Hungary
,
I. Wittmann
1   2nd Department of Medicine and Nephrological Center University of Pécs, Pécs, Hungary
,
G. A. Molnár
1   2nd Department of Medicine and Nephrological Center University of Pécs, Pécs, Hungary
› Author Affiliations
Further Information

Publication History

received 08 August 2015

accepted after seecond revision 20 January 2016

Publication Date:
14 March 2016 (online)

Abstract

Glucagon is known for its insulin-antagonist effect in the blood glucose homeostasis, while it also reduces vascular resistance. The mechanism of the vasoactive effect of glucagon has not been studied before; thereby we aimed to investigate the mediators involved in the vasodilatation induced by glucagon. The vasoactive effect of glucagon, insulin, and glucagon-like peptide-1 was studied on isolated rat thoracic aortic rings using a wire myograph. To investigate the mechanism of the vasodilatation caused by glucagon, we determined the role of the receptor for glucagon and the receptor for GLP-1, and studied also the effect of various inhibitors of gasotransmitters, inhibitors of reactive oxygen species formation, NADPH oxidase, prostaglandin synthesis, protein kinases, potassium channels, and an inhibitor of the Na+/Ca2+-exchanger. Glucagon causes dose-dependent relaxation in the rat thoracic aorta, which is as potent as that of insulin but greater than that of GLP-1 (7–36) amide. Vasodilatation by GLP-1 is partially mediated by the glucagon receptor. The vasodilatation due to glucagon evokes via the glucagon-receptor, but also via the receptor for GLP-1, and it is endothelium-independent. Contribution of gasotransmitters, prostaglandins, the NADPH oxidase enzyme, free radicals, potassium channels, and the Na+/Ca2+-exchanger is also significant. Glucagon causes dose-dependent relaxation of rat thoracic aorta in vitro, via the receptor for glucagon and the receptor for GLP-1, while the vasodilatation evoked by GLP-1 also evolves partially via the receptor for glucagon, thereby, a possible crosstalk between the 2 hormones and receptors could occur.

 
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