Please use this identifier to cite or link to this item: https://doi.org/10.1038/hr.2017.31
Title: A high-salt diet enhances leukocyte adhesion in association with kidney injury in young Dahl salt-sensitive rats
Authors: Takahashi, H
Nakagawa, S
Wu, Y
Kawabata, Y
Numabe, A
Yanagi, Y 
Tamaki, Y
Uehara, Y
Araie, M
Keywords: angiotensin receptor
creatinine
intercellular adhesion molecule 1
losartan
monocyte chemotactic protein 1
intercellular adhesion molecule 1
monocyte chemotactic protein 1
animal experiment
animal model
animal tissue
Article
controlled study
dietary intake
fluoroscopy
high salt diet
hypertension
kidney injury
leukocyte adherence
male
nonhuman
protein expression
rat
real time polymerase chain reaction
renin angiotensin aldosterone system
scanning laser ophthalmoscopy
animal
blood pressure
cell adhesion
Dahl rat
drug effect
kidney
kidney disease
leukocyte
metabolism
pharmacology
physiology
sodium intake
Animals
Blood Pressure
Cell Adhesion
Chemokine CCL2
Intercellular Adhesion Molecule-1
Kidney
Kidney Diseases
Leukocytes
Rats
Rats, Inbred Dahl
Sodium, Dietary
Issue Date: 2017
Publisher: Nature Publishing Group
Citation: Takahashi, H, Nakagawa, S, Wu, Y, Kawabata, Y, Numabe, A, Yanagi, Y, Tamaki, Y, Uehara, Y, Araie, M (2017). A high-salt diet enhances leukocyte adhesion in association with kidney injury in young Dahl salt-sensitive rats. Hypertension Research 40 (11) : 912-920. ScholarBank@NUS Repository. https://doi.org/10.1038/hr.2017.31
Rights: Attribution 4.0 International
Abstract: Salt-sensitive hypertension is associated with severe organ damage. Generating oxygen radicals is an integral component of salt-induced kidney damage, and activated leukocytes are important in oxygen radical biosynthesis. We hypothesized that a high-salt diet causes the upregulation of immune-related mechanisms, thereby contributing to the susceptibility of Dahl salt-sensitive rats to hypertensive kidney damage. For verifying the hypothesis, we investigated leukocytes adhering to retinal vessels when Dahl salt-sensitive rats were challenged with a high-salt (8% NaCl) diet using acridine orange fluoroscopy and a scanning laser ophthalmoscope. The high-salt diet increased leukocyte adhesion after 3 days and was associated with a significant increase in mRNA biosynthesis of monocyte chemotactic protein-1 and intercellular adhesion molecule-1 (ICAM-1) -related molecules in the kidney. Losartan treatment did not affect increased leukocyte adhesion during the early, pre-hypertensive phase of high salt loading; however, losartan attenuated the adhesion of leukocytes during the hypertensive stage. Moreover, the inhibition of leukocyte adhesion in the pre-hypertensive stage by anti-CD18 antibodies decreased tethering of leukocytes and was associated with the attenuation of functional and morphological kidney damage without affecting blood pressure elevation. In conclusion, a high-salt challenge rapidly increased leukocyte adhesion through the over-expression of ICAM-1. Increased leukocyte adhesion in the pre-hypertensive stage is responsible for subsequent kidney damage in Dahl salt-sensitive rats. Immune system involvement may be a key component that initiates kidney damage in a genetic model of salt-induced hypertension. © The Author(s) 2017.
Source Title: Hypertension Research
URI: https://scholarbank.nus.edu.sg/handle/10635/179080
ISSN: 09169636
DOI: 10.1038/hr.2017.31
Rights: Attribution 4.0 International
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