Premium
Early Supplementation of d ‐Cysteine or l ‐Cysteine Prevents Hypertension and Kidney Damage in Spontaneously Hypertensive Rats Exposed to High‐Salt Intake
Author(s) -
Hsu ChienNing,
Lin YuJu,
Lu PeiChen,
Tain YouLin
Publication year - 2018
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201700596
Subject(s) - medicine , kidney , endocrinology , oxidative stress , cysteine , angiotensin ii , chemistry , renin–angiotensin system , biochemistry , receptor , blood pressure , enzyme
Scope We investigate whether early supplementation of precursors of hydrogen sulfide (H 2 S), d‐ or l ‐cysteine can prevent hypertension and kidney damage in spontaneously hypertensive rats (SHR) treated with high‐salt. Methods and Results We examine 12‐week‐old male SHRs from four groups: SHR, high salt SHR (SHRs received 1% NaCl in drinking water for 8 weeks), high salt SHR+ d (SHRs received high salt and d‐ cysteine), and high salt SHR+ l (SHRs received high salt and l ‐cysteine). d‐ or l ‐cysteine was supplemented at 8 mmol kg −1 body weight/day between 4 and 6 weeks of ages. High salt intake exacerbate hypertension and kidney damage in SHRs, which is prevented by d‐ or l ‐cysteine supplementation. d‐ or l ‐Cysteine supplementation reduce the degree of high salt‐induced oxidative stress damage. Renal 3‐mercaptopyruvate sulphurtransferase (3MST) protein levels and activity are reduced by d‐ or l ‐cysteine supplementation. Additionally, d‐ or l ‐Cysteine supplementation reduce renal angiotensin I and angiotensin II concentrations, decrease mRNA expression of Ren , and increase protein levels of type 2 angiotensin II receptor. Conclusion Early supplementation of d ‐ or l ‐cysteine before hypertension becomes evident and may protect against hypertension and kidney damage in adult SHRs exposed to high salt consumption via regulation of oxidative stress, renin‐angiotensin system, and H 2 S‐generating pathways.