Hypoalbuminaemia enhances the renal vasoconstrictor effect of lysophosphatidylcholine.

Background: Lysophosphatidylcholine (LPC) causes vascular dysfunction in vitro. Lipoprotein LPC is increased in hypoalbuminaemia. Albumin binds LPC and restores LPC-induced abnormalities.

Hypoalbuminemia increases lysophosphatidylcholine in low-density lipoprotein of normocholesterolemic subjects.

Background: A phospholipid, lysophosphatidylcholine (LPC), is the major determinant of the atherosclerotic properties of oxidized low-density lipoprotein (LDL). Under normal circumstances most LPC is bound to albumin. We hypothesized that lipoprotein LPC concentrations are increased in hypoalbuminemic patients with the nephrotic syndrome, irrespective of their lipid levels.

Hypoalbuminemia causes high blood viscosity by increasing red cell lysophosphatidylcholine.

Albumin deficiency is accompanied by a reduction in red cell deformability and blood hyperviscosity. Albumin deficiency increases plasma fibrinogen and triglyceride levels and may alter red cell membrane lipid composition. These options, which could all contribute to reduced red cell deformability (RCD) and hyperviscosity, were studied in the Nagase analbuminemic rat (NAR), a mutant Sprague Dawley rat (CON), characterized by normal total protein levels, with an absolute deficiency of albumin, but elevated levels of non-albumin proteins and hyperlipidemia.

Proteinuria, lipoproteins and renal apolipoprotein deposits in uninephrectomized female analbuminemic rats.

To elucidate the pathogenetic role of hyperlipidemia per se in the development of glomerulosclerosis, severely hyperlipidemic female analbuminemic rats (NAR) and mildly hyperlipidemic male NAR were studied for a period of 37 weeks after uninephrectomy (UNX). Plasma cholesterol increased from 6.3 +/- 0.

Lipoprotein phospholipid composition and LCAT activity in nephrotic and analbuminemic rats.

Albumin is an acceptor of lysophosphatidylcholine (LPC), product of the lecithin:cholesterol acyl transferase (LCAT) reaction, and it has been suggested that low LCAT activity and reduced cholesterol esterification rate in patients with the nephrotic syndrome may be linked to depletion of albumin. Effects of low plasma albumin levels on LCAT activity, cholesterol esterification rates and LPC-binding were therefore studied in hyperlipidemic nephrotic (NS) and analbuminemic (NAR) rats. LPC-binding was also measured in normoalbuminemic rats with dietary hypercholesterolemia.

Subcutaneous administration of HMG-CoA reductase inhibitors in hyperlipidaemic and normal rats.

Recent reports demonstrate a hypocholesterolaemic effect of daily subcutaneous injections of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors in different rat models of hyperlipidaemia. However, this effect is not seen after oral administration of HMG-CoA reductase inhibitors in rats. We found that oral administration of the HMG-CoA reductase inhibitor Simvastatin also had no effect on plasma cholesterol in severely hyperlipidaemic Nagase analbuminaemic rats (NAR).

Hyperlipoproteinemia in one-year-old analbuminemic rats.

Plasma lipoprotein distribution and apolipoprotein concentrations, as well as kidney function and histopathology of heart, aorta, liver and kidney were investigated in 1-year-old Nagase analbuminemic rats (NAR) and control Sprague-Dawley rats (SDR). The NAR, particularly the females, were found to be severely hyperlipidemic. Plasma total cholesterol in non-fasted animals was 6.

Colloid osmotic pressure in young analbuminemic rats.

Colloid osmotic pressure (COP) was measured in plasma and interstitial fluid (subcutaneous wick) from 8 to 75 days of age in Nagase analbuminemic rats (NAR) and control Sprague-Dawley rats (SDR). In all animals plasma COP (approximately 10 mmHg at 8 days of age) increased during growth. In the female NAR the rise in nonalbumin proteins was so large that at 75 days the plasma COP was not lower than in the SDR; whereas in male NAR a difference of approximately 4 mmHg remained.

Plasma proteins in growing analbuminaemic rats fed on a diet of low-protein content.

1. Analbuminaemic and Sprague-Dawley (control) rats were fed on low- (60 g/kg) protein and control (200 g protein/kg) diets ad lib. from weaning.

Prolactin binding in benign and malignant mammary tissue of female dogs.

Prolactin receptor (PRL-R) concentrations were determined in membrane preparations of canine mammary tumours and of non-affected mammary tissues by a radioreceptor-assay using ovine prolactin (oPRL) both for 125I-labelling and for displacement. Receptor levels greater than or equal to 3 fmol/mg membrane protein were considered positive. Histologically non-affected samples of mammary tissue from 6 dogs were PRL-R positive (12-195 fmol/mg protein).