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Glucagon‐like peptide‐1 affects mean arterial pressure, renal blood flow and urinary flow rate in spontaneously hypertensive rats despite no renal expression of GLP‐1 receptors
Author(s) -
Sorensen Charlotte Mehlin,
Ronn Jonas,
Holst Jens Juul,
Jensen Elisa Pauline
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.701.10
Subject(s) - endocrinology , medicine , kidney , renal blood flow , renal circulation , renal function , blood pressure , vasodilation , mean arterial pressure , heart rate
Glucagon‐like peptide‐1 (GLP‐1) has many extrapancreatic effects and the GLP‐1 receptor is expressed in many tissues. GLP‐1 increases renal blood flow (RBF), glomerular filtration rate and sodium and water excretion. Also, GLP‐1 has been shown to reduce blood pressure in some hypertensive models. The aim of this study was to examine expression of the GLP‐1 receptor in the renal vasculature from spontaneously hypertensive rats (SHR) and to assess the renal and vascular effects of GLP‐1. Methods The GLP‐1 receptor was localized using both immunohistochemical staining and in situ hybridization for the GLP‐1 receptor on kidney sections from normotensive Sprague‐Dawley (SD) and hypertensive SHR rats. The vasodilatory effect of GLP‐1 was examined in isolated interlobar arteries. In vivo experiments were performed on rats monitoring mean arterial blood pressure (MAP), RBF, heart rate (HR), urine flow and sodium excretion. GLP‐1 was infused directly into the kidney for 20 min before and after infusion of the GLP‐1 receptor antagonist exendin9–39. Results No GLP‐1 receptor positive staining was found in kidneys from SHR whereas there was GLP‐1 receptor positive staining in the vascular smooth muscle cells in the renal vasculature from normotensive rats. No vasodilation was elicited in interlobar arteries from SHR whereas arteries from SD responded to increasing concentrations of GLP‐1. Intrarenal infusion of GLP‐1 increased BP, RBF, urine flow and sodium excretion significantly in both rat strains whereas heart rate was unchanged. The effect on RBF and MAP was abolished by exendin9–39 whereas the increase in urine flow and sodium excretion was still present. Conclusion The renal effects of GLP‐1 in SHR do not rely on the presence of renal GLP‐1 receptors. It seems likely that the GLP‐1 mediated effects in SHR are mediated via extrarenal GLP‐1 receptors e.g. GLP‐1 receptors in organs responsible for regulation of insulin or ANP.