ABSTRACT
The human uterotrophic placental factor (hUTPF) is a protein obtained from human term placentae and acts on uterine growth, mammary gland, and blastocyst development and implantation. In the present work, we further define some molecular characteristics of hUTPF using chromatographic, electrophoretic and immunochemical methods. It is concluded that in human term placenta a high molecular weight hUTPF is present, bound to albumin and immunoglobulins, which could represent a storage or transport form of this factor. hUTPF presents several molecular forms, one of them of 270 kDa and others of approximately 90 kDa and 27 kDa
Subject(s)
Animals , Female , Humans , Mice , Pregnancy , Pregnancy Proteins/chemistry , Uterus/chemistry , Blotting, Western/methods , Chromatography, Ion Exchange/methods , Concanavalin A , Electrophoresis, Polyacrylamide Gel/methods , Immunochemistry/methods , Mice, Inbred BALB C , Molecular Weight , Organ Size/drug effects , Placental Extracts/administration & dosage , Placental Extracts/pharmacology , Uterus/drug effects , Uterus/growth & developmentABSTRACT
Renal response to atrial natriuretic peptide in chronic cholestasis was studied in anaesthetized rats and in their isolated perfused kidneys. Cholestasis was induced by bile duct section after ligature, while controls were sham operated. Three weeks after surgery, cholestatic rats showed moderate arterial hypotension, elevated diuresis and no differences in urinary sodium, glomerular filtration rate (GFR) and fractional sodium excretion (FENa), when compared to controls. Isolated kidneys of cholestatic rats had equal basal diuresis and less natriuresis than the controls. Cholestatic rats presented blunted natriuretic and diuretic responses to iv injections of atrial natriuretic peptide (ANP 0.5 microgram), associated with reduced increments in GFR and FENa, when compared with controls. Similarly, the diuretic-natriuretic response of isolated kidneys to ANP (3.5 x 10(-9) M) was greatly attenuated in this group. ANP did not increase perfusion pressure in cholestatic rats, as it did in controls. These results indicate that animals with chronic cholestasis present refractoriness to ANP, which might be mediated by a direct impairment at the renal vascular and tubular sites for ANP action