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Hyperprolactinaemia in patients with chronic renal disease undergoing dialysis has prompted the investigation of the relative roles of liver and kidney in the degradation of prolactin. Male rabbits were acutely nephrectomized, and compared with intact animals with or without prolactin infusion. Prolactin degradation was followed after intravenous injection of ¹²⁵I-labelled ovine prolactin. Measurements were made of peptide-bound ¹²⁵I and ¹²⁵I-labelled degradation products in plasma, liver, kidney, bile, urine and muscle and total thyroid radioactivity. A significant (P<0·01) reduction in the metabolic clearance rate of ¹²⁵I-labelled prolactin was observed due to nephrectomy, with double the accumulation of ¹²⁵I-labelled peptides in the livers in this group. Prolactin infusion of nephrectomized animals had a further and larger effect than nephrectomy alone on prolactin degradation. Metabolic clearance rate significantly (P<0·01) decreased from 5·5 ml/min per kg in nephrectomized rabbits to 0·8 ml/min per kg with prolactin infusion. The accumulation of ¹²⁵I-labelled prolactin degradation products in the blood was significantly (P<0·01) lower in this group of animals and the amount of peptide-bound ¹²⁵I in plasma at 60 min after ¹²⁵I-labelled prolactin administration was significantly (P<0·01) higher. Liver degradation of prolactin in the absence of exogenous hormone appears to be sufficient to maintain an approximately normal half-life for prolactin in plasma (intact t = 6·8 min; nephrectomized t = 8·5 min). However, with prolactin infusion the half-life of ¹²⁵I-labelled prolactin increased to 28·5 min, and the plasma prolactin concentrations measured by radioimmunoassay rose linearly with time. These data supported the view that hyperprolactinaemia associated with renal dysfunction is substantially due to hormone oversecretion.