Open AccessGlucagon‐like peptide‐1 acutely affects renal blood flow and urinary flow rate in spontaneously hypertensive rats despite significantly reduced renal expression of GLP‐1 receptors
Author(s) -
Ronn Jonas,
Jensen Elisa P.,
Wewer Albrechtsen Nicolai J.,
Holst Jens Juul,
Sorensen Charlotte M.
Publication year - 2017
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.13503
Subject(s) - endocrinology , medicine , natriuresis , diuresis , renal blood flow , kidney , renal circulation , glucagon like peptide 1 , blood pressure , mean arterial pressure , diabetes mellitus , heart rate , type 2 diabetes
Abstract Glucagon‐like peptide‐1 (GLP‐1) is an incretin hormone increasing postprandial insulin release. GLP‐1 also induces diuresis and natriuresis in humans and rodents. The GLP‐1 receptor is extensively expressed in the renal vascular tree in normotensive rats where acute GLP‐1 treatment leads to increased mean arterial pressure (MAP) and increased renal blood flow (RBF). In hypertensive animal models, GLP‐1 has been reported both to increase and decrease MAP. The aim of this study was to examine expression of renal GLP‐1 receptors in spontaneously hypertensive rats (SHR) and to assess the effect of acute intrarenal infusion of GLP‐1. We hypothesized that GLP‐1 would increase diuresis and natriuresis and reduce MAP in SHR. Immunohistochemical staining and in situ hybridization for the GLP‐1 receptor were used to localize GLP‐1 receptors in the kidney. Sevoflurane‐anesthetized normotensive Sprague–Dawley rats and SHR received a 20 min intrarenal infusion of GLP‐1 and changes in MAP, RBF, heart rate, dieresis, and natriuresis were measured. The vasodilatory effect of GLP‐1 was assessed in isolated interlobar arteries from normo‐ and hypertensive rats. We found no expression of GLP‐1 receptors in the kidney from SHR. However, acute intrarenal infusion of GLP‐1 increased MAP, RBF, dieresis, and natriuresis without affecting heart rate in both rat strains. These results suggest that the acute renal effects of GLP‐1 in SHR are caused either by extrarenal GLP‐1 receptors activating other mechanisms (e.g., insulin) to induce the renal changes observed or possibly by an alternative renal GLP‐1 receptor.