Journalartikel
Autorenliste: Ross, Guenter; Heinemann, Marcus P.; Schlueter, Klaus-Dieter
Jahr der Veröffentlichung: 2007
Seiten: 878-886
Zeitschrift: Peptides
Bandnummer: 28
Heftnummer: 4
ISSN: 0196-9781
DOI Link: https://doi.org/10.1016/j.peptides.2006.12.010
Verlag: Elsevier
Abstract:
Tuberoinfundibular peptide of 39 residues (TIP39) is a member of the parathyroid hormone (PTH) family and a highly specific ligand of the PTH-receptor type 2 (PTH-2r). Recent studies have shown vasoactive properties of TIP39 in the kidney. This effect was stronger after desensitization of the parathyroid hormone-receptor type 1 (PTH-1r). The aims of our study were three-fold: (1) to investigate the influence of TIP39 on coronary resistance (CR), (2) to investigate a possible cross-talk between vascular PTH-receptors in the cardiovascular system, and (3) to investigate whether the endogenously released PTHrP during ischemia induces such a desensitizing effect. Experiments were performed on isolated rat hearts that were perfused with a constant pressure (Langendorff mode) and the coronary flow was determined. Under basal conditions, TIP39 showed no influences on CR. However, TIP39 reduced the CR by approximately 22% after pre-treatment of the hearts with a PTH-1r agonist. This TIP39 effect was abolished either by co-administration of a PTH-2r antagonist or by inhibition of nitric oxide (NO) formation. In an ischemia-reperfusion model endogenously released PTHrP desensitized the PTH-1r and pre-ischemic addition of TIP39 reduced post-ischemic CR by about 28%. Again, this effect was completely abolished in the presence of the PTH-2r antagonist or the PTH-1r-antagonist or by inhibition of NO formation. However, no effect was observed when TIP39 was washed-out prior to ischemia or if the treatment with TIP39 was restricted to the reperfusion. Furthermore, a pre-ischemic application of the NO-dependent vasorelaxant bradykinin provoked a similar effect on the post-ischemic CR than TIP39. In conclusion, a NO-dependent vasodilatory effect of TIP39 was demonstrated if the PTH-1r is desensitized by either exogenously applicated PTHrP peptides or endogenously released PTHrP. (c) 2007 Published by Elsevier Inc.
Zitierstile
Harvard-Zitierstil: Ross, G., Heinemann, M. and Schlueter, K. (2007) Vasodilatory effect of tuberoinfundibular peptide (TIP39):: Requirement of receptor desensitization and its beneficial effect in the post-ischemic heart, Peptides, 28(4), pp. 878-886. https://doi.org/10.1016/j.peptides.2006.12.010
APA-Zitierstil: Ross, G., Heinemann, M., & Schlueter, K. (2007). Vasodilatory effect of tuberoinfundibular peptide (TIP39):: Requirement of receptor desensitization and its beneficial effect in the post-ischemic heart. Peptides. 28(4), 878-886. https://doi.org/10.1016/j.peptides.2006.12.010
Schlagwörter
39 RESIDUES; CORONARY ENDOTHELIAL-CELLS; coronary system; HORMONE-RELATED PROTEIN; ISCHEMIA-REPERFUSION INJURY; KINASE-C; MESSENGER-RIBONUCLEIC-ACID; parathyroid hormone; PARATHYROID-HORMONE; parathyroid hormone-related protein; RAT-HEART; VASCULAR SMOOTH-MUSCLE; vasodilatory peptides