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Abstract P220: Congestive Heart Failure in the Rat Induces Subtle Renal Damage via Neurogenic Pathways

Authors :
Kerstin Amann
Roland E. Schmieder
Martin Hindermann
Sonja Heinlein
Karl F. Hilgers
Kristina Rodionova
Tilmann Ditting
Peter Linz
Christian Ott
Roland Veelken
Source :
Hypertension. 66
Publication Year :
2015
Publisher :
Ovid Technologies (Wolters Kluwer Health), 2015.

Abstract

Background: Cardiomyopathy in experimental renal insufficiency is putatively influenced by neurogenic pathways of renal origin. We wondered if cardiac neurogenic effects in congestive heart failure could likewise harm the kidney. We hypothesized that increased renal sympathetic nerve activity (RSNA) in rats with congestive heart failure after myocardial infarction (CHF) induces renal structural damage. Methods: 21 day after induction of CHF renal morphology was evaluated by immunohistology (interstitial and glomerular mononuclear cell infiltration (ED1), cell proliferation (PCNA), collagen I,III,IV,V,VI, laminin und fibronectin). RSNA was assessed by volume challenge (VE) to decrease RSNA. CHF and control rats were investigated with and without renal denervation (DNX). Blood pressure (BP), heart rate (HR) and RSNA were recorded. Nodose ganglion neurons (NGN) with vagal cardiac afferents were cultured for 1 day. Whole cell recordings were obtained and current-voltage relationships established. Cells were characterized by osmomechanical stress with a mannitol solution. Results: In CHF rats with intact renal nerves (nonDNX) formation of collagen I occurred, that was reduced after DNX (12.2+0.7 %area vs. 9.1+1.1 %area*, n=6, * p Conclusion: CHF induced subtle renal structural damage due to increased renal sympathetic tone which was likely due to altered NGN mechanosensitivity. Afferent nerve units from cardiovascular organs obviously form a complex sympathomodulatory network.

Details

ISSN :
15244563 and 0194911X
Volume :
66
Database :
OpenAIRE
Journal :
Hypertension
Accession number :
edsair.doi...........47f657e32404fa25f620d678de4c518f
Full Text :
https://doi.org/10.1161/hyp.66.suppl_1.p220