Key result
Decreased plasma angiotensinogen concentration in nephrotic rats is related to elevated plasma renin concentration and urinary angiotensinogen excretion rather than altered hepatic gene expression.
Why the study?
How do various hormonal and surgical treatments affect hepatic angiotensinogen gene expression and plasma angiotensinogen concentration in nephrotic versus control rats?
How do various hormonal and surgical treatments affect hepatic angiotensinogen gene expression and plasma angiotensinogen concentration in nephrotic versus control rats?
The study demonstrates that reduced plasma angiotensinogen in nephrotic rats is driven by increased urinary excretion and renin consumption rather than decreased hepatic gene expression.
Answers are grounded in this paper and cite their sources.
Reduced plasma angiotensinogen in nephrotic rats reflects urinary loss and renin consumption; leaves open mechanisms and relevance in human disease.
Plasma angiotensinogen (Ao) concentration (PAC), urinary Ao excretion (UAE), hepatic levels of Ao mRNA and plasma renin concentration (PRC) were studied in control and nephrotic rats subjected to the following treatments: dexamethasone (DEX), ethinyl-estradiol (EE), tri-iodothyronine (T3), bilateral nephrectomy (NX), captopril (CAP) and adrenalectomy (ADX). In nephrotic rats PAC diminished, UAE and PRC augmented and Ao mRNA levels were not altered. In control rats, DEX, EE, T3 and NX increased PAC and Ao mRNA levels whereas CAP diminished PAC but not affected Ao mRNA. ADX diminished PAC and Ao mRNA levels. In nephrotic rats, these treatments produced the same effect than in control rats except in ADX which did not affect PAC. These data suggest that the decreased PAC is not related to alterations in hepatic Ao gene expression but to elevated PRC and UAE.
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Medina-Campos et al. (1997) studied Nephrotic syndrome (in rats). Dexamethasone, ethinyl-estradiol, tri-iodothyronine, bilateral nephrectomy, captopril, and adrenalectomy vs. Control rats was evaluated on Plasma angiotensinogen concentration, urinary Ao excretion, hepatic levels of Ao mRNA, and plasma renin concentration. Decreased plasma angiotensinogen concentration in nephrotic rats is related to elevated plasma renin concentration and urinary angiotensinogen excretion rather than altered hepatic gene expression.
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