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Early Supplementation of d‐Cysteine or l‐Cysteine Prevents Hypertension and Kidney Damage in Spontaneously Hypertensive Rats Exposed to High‐Salt Intake
Scope
We investigate whether early supplementation of precursors of hydrogen sulfide (H2S), 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 H2S‐generating pathways.
High salt intake exacerbates hypertension and kidney damage in spontaneous hypertensive rats (SHRs), which is prevented by d‐ or l‐cysteine supplementation. d‐ or l‐cysteine supplementation decreases renal 3‐mercaptopyruvate sulphurtransferase (3MST) protein levels and activity, decreases mRNA expression of renin (Ren), and increased protein levels of angiotensin II type 2 receptor (AT2R). The protective roles of early supplementation of d‐ or l‐cysteine on hypertension and kidney injury through regulation of hydrogen sulfide (H2S), oxidative stress, and renin‐angiotensin system (RAS) pathways is shown.