Prolactin metabolism in the rat: role of the kidney in degradation of the hormone.
The contribution of impaired prolactin (PRL) degradation to the altered dynamics of this hormone in uremia was investigated in rats. Hyperprolactinemia developed after bilateral nephrectomy (BNx) or ligation of both ureters (BUL), whereas PRL levels remained normal in comparably azotemic animals undergoing urine autoinfusion in which glomerular filtration rate (GFR) was maintained. The renal organ clearance of PRL in control rats accounted for two-thirds of its metabolic clearance rate and was consistently less than GFR. Following BUL and BNx the metabolic clearance of PRL decreased predictably also by two-thirds. The importance of the renal parenchyma in the degradation of prolactin was confirmed during perfusion of isolated rat kidneys. Renal PRL handling involves mainly glomerular filtration and tubular reabsorption, although uptake from peritubular blood is also demonstrable under the high plasma flow conditions obtaining during in vitro kidney perfusion. We conclude that the hyperprolactinemia associated with acute uremia in the rat is not the consequence of the uremic state per se, but results from impaired renal degradation of the hormone.
D000818:Animals; D005919:Glomerular Filtration Rate; D066298:In Vitro Techniques; D007668:Kidney / Q000378:metabolism*; D008026:Ligation; D008297:Male; D008657:Metabolic Clearance Rate; D009392:Nephrectomy; D010477:Perfusion; D011388:Prolactin / Q000097:blood / Q000378:metabolism*; D051381:Rats; D014511:Uremia / Q000378:metabolism; D014513:Ureter / Q000502:physiology
D011388:Prolactin