Arginine vasopressin gene expression in rats with puromycin-induced nephrotic syndrome

Abstract Nephrotic syndrome is characterized by water and sodium retention, which leads to edema formation. The nonosmotic stimulation of arginine vasopressin (AVP) release from the pituitary gland has been implicated to be one of the important factors of abnormal water retention in patients with nephrotic syndrome. It is not known, however, whether nephrotic syndrome is associated with stimulation of hypothalamic vasopressin gene expression. Puromycin aminonucleoside is known to cause altered glomerular permeability, which results in experimental nephrotic syndrome in rats. In the present study, therefore, AVP gene expression has been studied in the hypothalamus of rats with puromycin aminonucleoside-induced nephrotic syndrome (PNS). Nephrotic syndrome was induced by a single intravenous injection of puromycin aminonucleoside (50 mg/kg body weight). Nephrotic syndrome was confirmed by urinary protein excretion (control 20.8 ± 3.5 mg/24 hr v PNS273.9 ± 41.4mg/24hr; P v PNS2.96 ± 0.22g/dL; P v PNS2.13 ± 0.42pg/mL; P 2 O v PNS290.3 ± 2.5mOsm/kg H 2 O; P = NS, n=12) or serum sodium concentration (control 142.7 ± 0.7 v PNS142.1 ± 1.1; PNS, n=12). Hypothalamic AVP mRNA determined by solution hybridization was significantly increased in PNS rats (control 2,915 ± 545 pg/hypothalamus v PNS5,914 ± 1,161pg/hypothalamus; P