High-salt intake accelerates functional and histological renal damage associated with renal tissue overexpression of (pro)renin receptors and AT1 receptors in spontaneously hypertensive rats

Autor: Yoshihisa Yamada, Kazuhiko Nishigaki, Yuka Hayakawa, Shingo Minatoguchi, Hiromitsu Kanamori, Shinya Minatoguchi, Hisaaki Komaki
Rok vydání: 2020
Předmět:
Nephrology
Male
medicine.medical_specialty
Physiology
Systole
030232 urology & nephrology
Angiotensinogen
Blood Pressure
Receptors
Cell Surface
030204 cardiovascular system & hematology
Kidney
Rats
Inbred WKY
p38 Mitogen-Activated Protein Kinases
Receptor
Angiotensin
Type 1
Blood Urea Nitrogen
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Physiology (medical)
Internal medicine
Rats
Inbred SHR
Renin–angiotensin system
medicine
Animals
cardiovascular diseases
Prorenin Receptor
Phosphorylation
Sodium Chloride
Dietary
Blood urea nitrogen
Creatinine
Angiotensin II receptor type 1
business.industry
Glomerulosclerosis
Focal Segmental
Body Weight
Glomerulosclerosis
medicine.disease
Fibrosis
Blood pressure
Endocrinology
medicine.anatomical_structure
chemistry
Hypertension
business
Signal Transduction
Zdroj: Clinical and experimental nephrology. 24(7)
ISSN: 1437-7799
Popis: This study aimed to investigate the effect of combination of high-salt intake and hypertension on renal functional and histological damage, associated with renal (pro)renin receptor [(P)RR] and AT1 receptor in rats. Wistar Kyoto rats (WKYs) and spontaneously hypertensive rats (SHRs) received regular rat chow (normal-salt diet 0.9%) or high-salt rat chow (high-salt diet 8.9%) for 6 weeks from 6 to 12 weeks of age. Systolic blood pressure, serum creatinine and blood urea nitrogen (BUN) were measured. Histological analysis of the kidney was performed. Western blot analysis was performed on the expressions of (P)RR, angiotensinogen and AT1 receptor in the kidney. High-salt intake significantly increased systolic blood pressure in WKYs and especially in SHRs. High-salt intake significantly increased serum creatinine and BUN, and accelerated renal tubulointerstitial fibrosis and glomerular sclerosis in SHRs. High-salt intake significantly enhanced the renal tissue expressions of (P)RR, angiotensinogen and AT1 receptor in SHRs. High-salt intake accelerates functional and histological renal damage associated with renal tissue overexpression of (P)RR and AT1 receptors in SHRs.
Databáze: OpenAIRE
Externí odkaz: