Natriuretic peptide (NP) genes are expressed in kidney. We have recently shown that renal NP gene expression can be upregulated in a setting where absolute sodium excretion (UnaV) per nephron is increased, i.e., 5/6 nephrectomy (Totsune etalJ Am See Neph 1995:6:749). The present study was undertaken to determine whether renal NP gene expression is upregulated under a condition in which plasma ANP is high yet llMaV/nephron is decreased. In heart failure, despite increased circulating NP activity which helps to maintain Na excretion (Zhang el a/Circ Res 1995:77:1240), UNaV/nephron is still low. Renal ANP mRNA expression was studied in rats subjected to coronary ligation causing left ventricular infarction and congestive heart failure (CHF), or shamoperated (SO) control rats (each: ri=4). At 3 to 4 weeks after surgery, rats were anesthetized, arterial blood was collected and cardiac atria and kidneys were harvested. ANP mRNA concentration was determined using a competitive quantitative RT-PCR method in kidneys and Northern blot in atrial tissue. Plasma ANP levels averaged > 14-fold higher in CHF vs. SO rats. Atrial ANP mRNA expression was also significantly increased in CHF rats (x1.38±0.09, mearttSE, p<0.05) when compared to SO controls. However, no significant upregulation of renal ANP mRNA expression was observed in CHF vs. SO rats (p>0.2, f-test). These data suggest that in heart failure upregulation of renal ANP gene expression is dissociated from cardiac gene expression and circulating ANP levels. Moreover, low level renal ANP gene expression correlates closely with low UNaV/nephron. Thus, locally synthesized peptide may be the primary mediator of natriuresis per nephron.
|ジャーナル||Journal of Investigative Medicine|
|出版ステータス||Published - 1996 1 1|
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