Impaired responsiveness of renal sensory nerves in streptozotocin-treated rats and obese Zucker diabetic fatty rats: role of angiotensin

Ulla C Kopp; Michael Z Cicha; Mark A Yorek

doi:10.1152/ajpregu.00830.2007

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Impaired responsiveness of renal sensory nerves in streptozotocin-treated rats and obese Zucker diabetic fatty rats: role of angiotensin

Journal article

Peer reviewed

Impaired responsiveness of renal sensory nerves in streptozotocin-treated rats and obese Zucker diabetic fatty rats: role of angiotensin

Ulla C Kopp, Michael Z Cicha and Mark A Yorek

American journal of physiology. Regulatory, integrative and comparative physiology, Vol.294(3), pp.R858-866

03/2008

DOI: 10.1152/ajpregu.00830.2007

PMID: 18199587

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Abstract

Increasing afferent renal nerve activity decreases efferent renal nerve activity and increases urinary sodium excretion. Activation of renal pelvic mechanosensory nerves is impaired in streptozotocin (STZ)-treated rats (model of type 1 diabetes). Decreased activation of renal sensory nerves would lead to increased efferent renal nerve activity, sodium retention, and hypertension. We examined whether the reduced activation of renal sensory nerves in STZ rats was due to increased renal angiotensin activity and whether activation of the renal sensory nerves was impaired in obese Zucker diabetic fatty (ZDF) rats (model of type 2 diabetes). In an isolated renal pelvic wall preparation from rats treated with STZ for 2 wk, PGE2 failed to increase the release of substance P, from 5 +/- 1 to 6 +/- 1 pg/min. In pelvises from sham STZ rats, PGE2 increased substance P release from 6 +/- 1 to 13 +/- 2 pg/min. Adding losartan to the incubation bath increased PGE2-mediated release of substance P in STZ rats, from 5 +/- 1 to 10 +/- 2 pg/min, but had no effect in sham STZ rats. In pelvises from obese ZDF rats (22-46 wk old), PGE2 increased substance P release from 12.0 +/- 1.2 to 18.3 +/- 1.2 pg/min, which was less than that from lean ZDF rats (10.3 +/- 1.6 to 22.5 +/- 2.4 pg/min). Losartan had no effect on the PGE2-mediated substance P release in obese or lean ZDF rats. We conclude that the mechanisms involved in the decreased responsiveness of the renal sensory nerves in STZ rats involve activation of the renin angiotensin system in STZ but not in obese ZDF rats.

Kidney - physiology

Neurons, Afferent - drug effects

Dinoprostone - pharmacology

Kidney - drug effects

Capsaicin - pharmacology

Angiotensins - physiology

Losartan - pharmacology

Rats

Male

Angiotensin II Type 1 Receptor Blockers - pharmacology

Neurons, Afferent - physiology

Obesity - genetics

Rats, Sprague-Dawley

Obesity - pathology

Baroreflex - drug effects

Rats, Zucker

Animals

Mechanoreceptors - drug effects

Diabetes Mellitus, Experimental - pathology

Kidney - innervation

Substance P - metabolism

Details

Title: Subtitle: Impaired responsiveness of renal sensory nerves in streptozotocin-treated rats and obese Zucker diabetic fatty rats: role of angiotensin
Creators: Ulla C Kopp - Department of Internal Medicine, Department of Veterans Affairs Medical Center, Bldg. 41, Rm 124, Highway 6W, Iowa City, IA 52246, USA. ulla-kopp@uiowa.edu
Michael Z Cicha
Mark A Yorek
Resource Type: Journal article
Publication Details: American journal of physiology. Regulatory, integrative and comparative physiology, Vol.294(3), pp.R858-866
DOI: 10.1152/ajpregu.00830.2007
PMID: 18199587
ISSN: 0363-6119
eISSN: 1522-1490
Grant note: R56 DK073990 / NIDDK NIH HHS R01-HL-66068 / NHLBI NIH HHS DK-073990 / NIDDK NIH HHS
Language: English
Date published: 03/2008
Academic Unit: Fraternal Order of Eagles Diabetes Research Center; Neuroscience and Pharmacology; Nephrology; Endocrinology and Metabolism; Internal Medicine
Record Identifier: 9984094711402771

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