Renoprotective Effects of Soy Protein Hydrolysates in N.OMEGA.-Nitro-L-Arginine Methyl Ester Hydrochloride-Induced Hypertensive Rats

Abstract

Pepsin-digested soy protein hydrolysate (SPH) has been reported to be responsible for many of the physiological benefits associated with soy protein consumption. In the present study, we investigated the effects of SPH with angiotensin-converting enzyme (ACE) inhibitory potential on blood pressure and renal injuries in rats with N -nitro-L -arginine methyl ester hydrochloride (L-NAME)-induced hypertension. Rats were fed a diet containing L-NAME (50 mg/kg body weight) with or without SPH (at 1%, 3%, or 5%) for 6 weeks. We found that ingestion of SPH ameliorated the development of hypertension during the 6-week experimental period. SPH was also found to ameliorate renal function by decreasing urinary protein excretion and elevating the creatinine clearance rate. The levels of kidney ACE activity, malonaldehyde, tumor necrosis factorand plasminogen activator inhibitor-1, and the expression of CYP4A decreased in the 5% SPH group. Consumption of 5% SPH also ameliorated renal damage according to the histopathological analysis. These find-

Preventive effects of aqueous extract of the whole plant of Eleusine indica (Linn) Gaertn. (Poaceae) against L-NAME induced nephrotoxicity in rat

“…We observed a significant increase in serum level of potassium, with a significant depletion in sodium level in L-NAME treated rats as compared to controls. These results are different to those obtained by Yang and Chen [3] . The decrease of Na + and the increase of K + observed in this study are probably due to the generation of free radicals and the inhibition of Na + -K + ATPase pump.…”

“…The bioavailability depletion of this molecule contributes to the impairment of cardiovascular function which leads to the activation of the renin-angiotensin system (RAS) and consequently angiotensin II production [2] . Angiotensin II causes inflammation, production of reactive oxygen species, blood pressure elevation and may also be involved in hypertension-induced tissue damage [3] . Uncontrolled hypertension with associated endothelial damage leads to progressive renal function impairment in essential hypertension and increases cardiovascular morbidity and mortality [4] .…”

Exposure to a “safe” dose of environmental pollutant bisphenol A elevates oxidative stress and modulates vasoactive system in hypertensive rats

“…43 An earlier study also indicates that anti-hypertensive and renoprotective effects of protective agents in nitric oxide (NO)-deficient rats might be mediated via its ACE inhibitory activity. 44 Strikingly, the adverse effect of the safe dose of BPA on oxidative stress, nitric oxide metabolism, and vasoactive factors that played crucial role in cardiovascular physiology was observed only under hypertensive milieu which requires further consideration.…”

The renoprotective effects of soy protein in the aging kidney

“…Given that CKD is a prototypical example of progressive fibrosis leading to organ failure [33], it is not surpising that the renoprotective effects of soy correlate with reduced fibrosis. In animal models [15,34], and clinical studies [19,35,36], soy has been shown to have an anti-inflammatory impact, including a reduction in NF-kB activity [15,16]. Given the emerging link between inflammation and renal fibrosis [37], this suggests that the anti-inflammatory effect of soy may underlie the reduction in fibrosis observed.…”