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<0.05). VE-induced RSNA decreases were impaired in CHF vs controls suggesting increased RSNA (-α 34+8% vs. -α[[Unable to Display Character: &#61472;]]54+6% *, n=6, * p<0.05). NGN from CHF exhibited altered conductance in response to mechanical stress as compared to controls (change in holding current at -80 mV: control_normoosmotic: -144±30 pA; control_hypoos.: -282±34 pA vs CHF_normosmotic: - 230±55 pA; CHF_hypos.: -540±100* pA; *p<0.05 CHF vs. control). 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.
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