Effects of renal denervation on renal pelvic contractions and connexin expression in rats

Koenen, Anna; Steinbach, Antje; Schaper, Katrin; Zimmermann, Uwe; Miehe, Bärbel; Kurt, Birgül; Rettig, Rainer; Grisk, Olaf

doi:10.1111/apha.12612

Cited by 2 publications

(1 citation statement)

References 38 publications

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“…IL-6, IFNγ, TNF-α and CM-GSF) compared to the contralateral control kidney. Unilateral denervation reportedly increases ipsilateral pelvic pressure, putatively due an enhanced diuresis 43 . The diuretic effect is likely mediated by a combination of decreased renal vascular resistance and decreased sodium/water reabsorption in the proximal tubule following unilateral RDN, both of which are maintained by renal sympathetic nerve discharge [44][45][46] .…”

Section: Differential Effect Of Renal Denervation On Renal Pro-inflammentioning

confidence: 95%

Renal Inflammation in DOCA-Salt Hypertension

et al. 2019

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Recent reports indicate that, in addition to treating hypertension, renal denervation (RDN) also mitigates renal inflammation. However, since RDN decreases renal perfusion pressure, it is unclear whether these effects are due to the direct effects of RDN on inflammatory signaling or secondary to decreased arterial pressure (AP). Therefore, this study was conducted to elucidate the contribution of renal nerves to renal inflammation in the DOCA-salt rat, a model in which RDN decreases AP and abolishes renal inflammation. In Experiment 1, we assessed the temporal changes in renal inflammation by measuring renal cytokines and AP in DOCA-salt rats. Uninephrectomized (1K) adult male Sprague Dawley rats that received surgical renal denervation (RDN) or sham (Sham) were administered DOCA (100mg, s.c.) and 0.9% saline for 21 days. AP was measured by radiotelemetry, and urinary cytokine excretion were measured repeatedly. In Experiment 2, the contribution of renal nerves in renal inflammation was assessed in a 2-kidney DOCA-salt rat to control for renal perfusion pressure. DOCA-salt treatment was administered after unilateral (U-)RDN. In Experiment 1, DOCA-salt induced increases in AP and renal inflammation (assessed by urinary cytokines) were attenuated by RDN versus Sham. In Experiment 2, GRO/KC, MCP-1, and macrophage infiltration were lower in the denervated kidney vs. the contralateral Sham kidney. No differences in T-cell infiltration were observed. Together, these data support the hypothesis that renal nerves mediate, in part, the development of renal inflammation in the DOCA-salt rat independent of hypertension. The mechanisms and cellspecificity mediating these effects require further investigation.

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Section: Differential Effect Of Renal Denervation On Renal Pro-inflammentioning

confidence: 95%

Renal Inflammation in DOCA-Salt Hypertension

et al. 2019

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Role of endothelin-1 for the regulation of renal pelvic function

Steinbach

Schaper

Koenen

et al. 2016

Pflugers Arch - Eur J Physiol

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Endothelin-1 (ET-1) stimulates contractions in isolated rat renal pelves. The signal transduction mechanisms that mediate ET-1-induced renal pelvic contractions and the role of ET-1 for the in vivo regulation of renal pelvic function are not well characterized. We tested if ET-1 stimulates contractions in murine and human renal pelves, if ET-1 activates the renal pelvic RhoA/ROCK pathway, and if low renal ET-1 formation or ET receptor blockade reduce renal pelvic contractile activity. ET-1 increased contraction frequency and force in murine renal pelves. The majority of human renal pelvic tissue samples showed tonic contractions in response to ET-1. Seven out of 20 human tissue samples showed phasic contractions. In four samples, they were elicited by ET-1 at 10-33 nmol/l. ET-1 increased renal pelvic RhoA-GTP content and myosin phosphatase target subunit 1 phosphorylation in isolated rat renal pelves. Renal pelvic contraction frequency (29 ± 2 vs. 29 ± 3 min(-1)) and renal pelvic pressure (7.1 ± 0.9 vs. 5.9 ± 1.7 mmHg) were similar in collecting duct-specific ET-1 knockout mice and in ET-1 floxed controls in vivo. ET-1 sensitivity of isolated renal pelves was similar in both groups. ET receptor blockade did not significantly affect pelvic contraction frequency and pressure in rats. We conclude that ET-1 stimulates phasic contractions in murine, rat, and, to a lesser extent, in human renal pelves. ET-1 activates the RhoA/ROCK pathway in the renal pelvic wall. Endogenous, kidney-derived ET-1 does not play a major role for the regulation of renal pelvic contractions in vivo.

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Effects of renal denervation on renal pelvic contractions and connexin expression in rats

Cited by 2 publications

References 38 publications

Renal Inflammation in DOCA-Salt Hypertension

Renal Inflammation in DOCA-Salt Hypertension

Role of endothelin-1 for the regulation of renal pelvic function

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