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Biomedical subjects

G Desoye

Publications and source records attributed to G Desoye.

At least 55 records · Page 3Linked to original sources
PubMed1995

[Pathogenesis and diagnosis of polycystic ovary syndrome].

OBJECTIVE: Growth factors (human growth hormone, HGH; insulin-like growth factor I, IGF-I) and insulin were evaluated concerning their pathogenetic significance in patients with polycystic ovary syndrome (PCOS). METHODS: Twenty-eight women with signs of PCOS were examined; 24 women without signs of PCOS served as controls. RESULTS: Women with PCOS showed significantly increased androgen, IGF-I, insulin and glucose levels, higher glucose concentrations in the oral glucose tolerance test and a higher body mass index. The concentration of HGH, the HGH/IGF-I ratio and the number of insulin receptors on red blood cells were significantly decreased in women with PCOS. The insulin receptor affinity, the maximum binding and the insulin-receptor complex were increased in PCOS patients. CONCLUSION: A decreased number of insulin receptors, a disturbed insulin receptor binding, the resulting hyperinsulinemia as well as high levels of IGF-I are to be considered as important factors in the pathogenesis of PCOS.

Adolescent↗
PubMed1995

[Secretion of endothelin-1 by trophoblast cells and binding of endothelin-1 to trophoblast membranes in healthy and pre-eclampsia pregnancies].

OBJECTIVES: The hypothesis was tested that the synthesis or binding of endothelin-1 (ET-1) by the trophoblast are altered in preeclampsia. METHODS: Trophoblast cells (TC) were isolated from 15 normal (C) und 18 pre-eclamptic pregnancies (P). Binding of [125I]ET-1 to plasma membranes of TC was determined after 48 h in culture. Concentration of ET-1 in culture media were measured after each 24 h over 5 day culture period. RESULTS: Specific binding was 150% (week 37-40) - 400% (week 31-36) higher (P < 0.01) in P. In contrast, the release of ET-1 was 60% (week 31-36) - 71% (week 37-40) lower (P < 0.01) in P than in healthy controls. CONCLUSIONS: Pre-eclampsia is associated with a lower release and increased binding of ET-1 by trophoblast cells.

Adult↗
PubMed1994

Insulin receptors in syncytiotrophoblast and fetal endothelium of human placenta. Immunohistochemical evidence for developmental changes in distribution pattern.

The localisation of insulin receptors (IR) was investigated on cryosections of human non-pathologic first trimester and full term placentae by indirect immunohistochemistry with three different monoclonal antibodies (MABS). In placentae from 6 to 10 weeks postmenstruation (p-m.), only syncytiotrophoblast was stained, predominantly that of mesenchymal villi and syncytial sprouts, which are areas of high proliferative activity. In placentae from 11 to 14 weeks p-m., endothelial cells commenced to react with the IR MABS and the syncytiotrophoblast was less intensely labelled than at weeks 6 to 10 p-m. In term placentae, the microvillous membrane of the syncytiotrophoblast showed only patches of weak immunoreactivity. In contrast, the endothelial cells in the placenta but not in the umbilical cord were strongly stained. The amniotic epithelium in the chorionic plate and fibroblasts in the stroma were conspicuously labelled. The data indicate: (1) the receptor density on villous syncytiotrophoblast decreases and that of fetal endothelium increases' throughout gestation; (2) syncytiotrophoblast of human term placentae expresses a low level per unit area of surface IR; and (3) the majority of IR in human term placentae is located in fetal endothelium. Apart from yet unknown functional effects of maternal and fetal insulin at the placental barrier, the results suggest a growth promoting effect on the trophoblast of maternal insulin in first trimester as well as developmental effects of fetal insulin on the feto-placental vessels at term.

Antibodies, Monoclonal↗
PubMed1994

Heterogeneous histochemical reaction pattern of the lectin Bandeiraea (Griffonia) simplicifolia with blood vessels of human full-term placenta.

Bandeiraea simplicifolia lectin (BS-I) stains vascular endothelium in various species. In humans, less than 10% of the specimens studied exhibit a reaction with BS-I. In the present histochemical study, the reactivity of BS-I with placental blood vessels and its correlation with the blood group from mother and newborn child was investigated. Acetone-fixed cryosections of representative tissue segments of human full-term placenta and umbilical cord were stained with BS-I. The staining pattern of tissues from patients with different blood groups was identical, although the reaction of BS-I in the placenta was heterogeneous. BS-I did not react with the umbilical cord. Vascular smooth muscle cells at the insertion site of the umbilical cord into the chorionic plate, and endothelium deeper in the chorionic plate, became progressively stained. The endothelial cells and tunica muscularis of smaller arteries and veins in stem villi lost their reactivity in parallel with decreasing vessel size. Arterioles and venules reacted heterogeneously. Capillaries, trophoblastic basement membranes, especially epithelial plates, and sometimes the syncytiotrophoblast were labelled in several terminal villi. The data indicate that 1) the placenta binds BS-I to fetal endothelium independent of the blood group, 2) cell-surface antigens on placental endothelial cells are expressed heterogeneously and 3) cell-surface glycans are constituted in an organ-specific manner on human endothelial cells.

Endothelium, Vascular↗
PubMed1994

Effects of the synthetic glucocorticoid triamcinolone acetonide on vasoactive hydrolases of the human placenta in vitro.

Therapy with glucocorticoids during pregnancy is still debated. Previously reported effects of glucocorticoid application in rats resemble certain symptoms of preeclampsia. Therefore, we studied in vitro the effects of the synthetic glucocorticoid triamcinolone acetonide soluble (0.1-10 mM) on placental alpha-glutamyl amino-peptidase, microsomal alanyl aminopeptidase, dipeptidyl peptidase IV, acetylcholinesterase and butyrylcholinesterase in purified trophoblast monolayers and villous explants from first trimester (n = 5) and term placentae (n = 9) using bio- and histochemical methods. In term placentae quantitative histochemistry (microdensitometry) of trophoblast monolayers revealed an increase of alpha-glutamyl aminopeptidase and microsomal alanyl aminopeptidase activity up to 149% and 126% respectively, after treatment with supraphysiological doses. In trophoblast monolayers from first trimester alpha-glutamyl aminopeptidase activity was not affected, whereas microsomal alanyl aminopeptidase activity increased by 25%. Dipeptidyl peptidase IV staining was reduced to 26%. Biochemical measurements of alpha-glutamyl aminopeptidase and microsomal alanyl aminopeptidase activity in homogenates of cultured villi revealed effects similar to those found by microdensitometry in trophoblast monolayers. In contrast, dipeptidyl peptidase IV activity increased in explants of term placentae by 47%. Acetyl- and butyrylcholinesterase activities were reduced in term placental villi by 38% and 40%, respectively. The data indicate that glucocorticoids may affect the activity of hydrolases which are thought to be involved in local placental blood pressure modulation.

Acetylcholinesterase↗
PubMed1994

Immunohistochemistry of two different types of placental fibrinoid.

The structure and composition of human placental fibrinoid were studied on cryostat and paraffin sections and by transmission electron microscopy as well as immunohistochemistry using antibodies directed against fibrin, fibronectin isoforms, collagens IV and VI, laminin and tenascin. The findings suggest two structurally and immunohistochemically different subtypes of fibrinoid: fibrin-type fibrinoid and matrix-type fibrinoid. Fibrin-type fibrinoid was characterized by immunoreactivity for fibrin and cellular fibronectin, including the ED-A sequence. Immunostaining for all other extracellular matrix molecules was negative. Ultrastructurally, this fibrinoid subtype consisted of a meshwork of fibers with 20-nm cross striation typical of fibrin. Fibrin-type fibrinoid never contained extravillous trophoblast cells. It is therefore primarily a blood clot product derived from maternal and fetal blood. In contrast, matrix-type fibrinoid showed virtually no evidence of fibrin; it was immunopositive for extracellular matrix molecules such as the fibronectins, particularly oncofetal fibronectin (containing the ED-B sequence), collagen IV, laminin and tenascin. Oncofetal fibronectin, which was neither expressed in fibrin-type fibrinoid nor in the villous stromal core, seemed to be a specific marker for matrix-type fibrinoid. Single or clustered nonproliferative extravillous trophoblast cells were embedded within the matrix molecules. It is very likely that these cells secrete the matrix in a non-polarized fashion. Fibrin-type fibrinoid would appear to be involved in shaping the intervillous space and in replacing damaged syncytiotrophoblast acting as a transport and immune barrier. Matrix-type fibrinoid, as a secretory product of the extravillous trophoblast, should be discussed in context with the invasive properties of this cell population.

Cell Adhesion Molecules, Neuronal↗
PubMed1994

Differential lectin binding to the fibrinoid of human full-term placenta: correlation with a fibrin antibody and the PAF-Halmi method.

Placental fibrinoid is thought to contain various glycoproteins originating from cell secretion and tissue degeneration, occasionally merged with fibrin. Information on the characteristics and derivation of the various fibrinoid components, however, is still fragmentary. Therefore, the present histochemical study on acetone-fixed placental tissue sections compared the staining pattern of FITC-conjugated lectins from Ulex europaeus (UEA-I), Bandeiraea simplicifolia (BS-I) and Lycopersicon esculentum (LEA) with the reactivity of a fibrin antibody and a modified paraldehyde-fuchsin stain. Using different color reactions, the latter histological method identified two types of fibrinoid, which correlated well with fibrin-type and matrix-type fibrinoid. Immunohistochemically, fibrin was detected at the intervillous border of the basal plate, in some inner parts and in perivillous fibrinoid. UEA-I bound to endothelial cells and partially to fibrin-type fibrinoid of villi and the basal plate, thus indicating a reaction with immured and disintegrated remnants of endothelial and blood cells. LEA stained fibrin-negative (i.e. matrix-type) fibrinoid homogeneously within the basal plate; the small reactive areas within the perivillous fibrinoid may belong to degenerating trophoblastic residues, because in villi LEA specifically reacted with the syncytiotrophoblast. BS-I heterogeneously labeled matrix-type fibrinoid deposits in the basal plate which surrounded decidual cells and subpopulations of extravillous trophoblast. In cell islands, BS-I also stained fibrinoid surrounding trophoblast cells heterogeneously. The data (1) confirm the existence of two types of placental fibrinoid, fibrin-type and matrix-type fibrinoid, (2) suggest that both types of fibrinoid contain different glycoconjugates, and (3) demonstrate the practical usefulness of the modified paraldehyde-fuchsin method for the identification of the two types of fibrinoid.

Endothelium, Vascular↗
PubMed1994

Non-Michaelis-Menten kinetics of zero-trans glucose uptake by trophoblast cells from human term placentae and by choriocarcinoma (JEG-3/JAR) cells.

Maternal glucose is a major substrate for placental and fetal metabolism. The kinetics of its uptake into placental trophoblast cells has not been characterised yet and was therefore investigated in the present study. In addition to trophoblast cells isolated from human term placentae, JEG-3 and JAR choriocarcinoma cells were used. Measurements were carried out in 5 s intervals until 30 s with the non-metabolisable glucose analogue 3-O-[14C]methyl-D-glucose using confluent cells adhering to glass coverslips. L-[1-14C]glucose was used to correct for extracellular trapped tracer and diffusion. The uptake was rapid and saturable. It reached equilibrium after 30 s at 20 degrees C and could be inhibited by 0.4 mmol/l cytochalasin B up to 98%. The choriocarcinoma cells took up twice as much glucose as trophoblast cells. Fitting the experimental data to the Michaelis-Menten equation by non-linear regression failed to adequately describe the data, even when a contribution of diffusion to total uptake was considered. Introducing the Hill coefficient n into the Michaelis-Menten equation significantly improved the quality of the fits as was assessed by three statistical criteria. Using this equation modified for allosteric kinetics (v = k[To] [S]n)/(Km + [S]n)), parameters were calculated as Km = 12 mmol/l, Vmax = 17 fmol/l s-1 per cell, n = 1.1 for trophoblast cells; Km = 13 mmol/l, Vmax = 27 fmol/l s-1 per cell, n = 1.2 for JEG-3 cells and Km = 29 mmol/l, Vmax = fmol/l s-1 per cell, n = 1.4 for JAR cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Adhesion↗
PubMed1993

Insulin receptor binding to erythrocytes in the first half of pregnancy is increased in healthy pregnant women as compared with non-pregnant or gestational diabetic women.

Insulin binding to erythrocytes was measured longitudinally by a competitive radioreceptor assay in 21 healthy pregnant (HP) and 20 well-controlled gestational diabetic women (GD) in 4-week intervals throughout pregnancy and at day 4 post-partum. Maximum insulin binding (maxbdg) at weeks 8-14 was increased (P < 0.001) in HP (median: 6.0%) but not in GD (median: 2.7%) as compared with non-pregnant control subjects (C) (median: 3.6%; previously reported: Clin. Chim. Acta 1992;207:57-71) due to an increased number of high-affinity insulin receptors. Throughout gestation the binding decreased continuously, to reach at term the levels found in C. In GD maxbdg remained close to the level of C throughout pregnancy. Binding differences between HP and GD were independent of the body mass index. Maxbdg did not differ between diet- and insulin-treated patients. It was higher in women whose offspring had low umbilical cord insulin levels (< 10 mu units/ml). The findings suggest that (a) higher insulin binding in HP could contribute to the improved glucose tolerance in early pregnancy and (b) the lack of increase in insulin binding during early pregnancy in gestational diabetes might be one factor leading to the manifestation of the disease in late pregnancy. However, it must be kept in mind that insulin receptors on erythrocytes do not necessarily resemble those on the major target tissues of insulin.

Adult↗
PubMed1993

Increase in insulin binding and inhibition of the decrease in the phospholipid content of human term placental homogenates in culture by the sulfonylurea glipizide.

Term placental explants were cultivated for 48 hr without (control) and with various concentrations of glipizide. Maximum binding of [125I]-insulin in the control samples was decreased after 12 and 24 hr returning to initial values after 48 hr. In the presence of glipizide the binding was generally higher, reaching 180% (557 and 1000 nmol/L) of the corresponding control value (P < 0.01) after 48 hr owing to the presence of nearly 3-fold more (P < 0.05) receptors than in the untreated controls. Tissue cholesterol content was almost unaffected whereas both the phospholipid content and the corresponding phospholipid-to-cholesterol ratios were markedly, and in a time-dependent manner, increased by glipizide as compared to the controls. This was due to decreasing cholesterol and phospholipid concentrations in the controls during the time of culture as compared to initial values, and also to unchanged levels in glipizide-treated cultures. We conclude that glipizide affects placental insulin receptors and the phospholipid content of the tissue.

Binding, Competitive↗
PubMed1993

Location and activities of acetylcholinesterase and butyrylcholinesterase in the rat and human placenta.

The location and physiological functions of acetylcholinesterase and butyrylcholinesterase in the placenta are still debated. In the present study the activities of both enzymes were studied histochemically in the rat and human placenta, using an optimized Karnovsky/Roots method. Additionally, they were measured biochemically. Acetylcholinesterase was active in the syncytiotrophoblast, cytotrophoplast cells and the visceral and parietal yolk sac epithelial cells of the rat (n = 10) and in the syncytiotrophoblast, cytotrophoblast cells, endothelial cells and the media of fetal blood vessels of the human placenta (n = 9). Butyrylcholinesterase could not be detected histochemically. Biochemically measured levels at certain developmental stages of the placenta revealed maximum acetylcholinesterase activity in the 8th week p.m. human placentae (102.9 nmol.min-1 per mg protein), 35% lower activity in the 12th week p.m., and minimum (44.1 nmol.min-1 per mg protein) in term placentae. In contrast, maximum butyrylcholinesterase activity was measured in week 12 p.m. (106.9 nmol.min-1 per mg protein). In rat placentae, butyrylcholinesterase activity on gestational day 21 reached 150% of the level on gestational day 16. Acetylcholinesterase activity remained constant. In placentae of pre-eclamptic patients, acetylcholinesterase and butyrylcholinesterase activities were found to be increased by 16% and 45%, respectively. The results suggest that placental acetylcholinesterase can no longer be considered as derived from maternal blood, but is primarily located within rat and human placental tissue.

Acetylcholinesterase↗
PubMed1993

Immunohistochemical localization of glucose transporters and insulin receptors in human fetal membranes at term.

The localization has been investigated of the isoforms GLUT1, GLUT3 and GLUT4 of glucose transporter proteins as well as of insulin receptors. Fetal membranes (n = 10) were examined by immunohistochemical methods at the light and electron microscopic levels using mono- and polyclonal antibodies. In all amnion epithelial cells, GLUT1 and GLUT3 antibodies were bound to the apical membrane. Very rarely the GLUT1 antibody also immunostained the basolateral membrane and reacted weakly with the endomembrane system and membranes of the lateral cell protrusions. Fibroblasts reacted with the antibodies against GLUT1, GLUT4 and insulin receptor, whereas they were labelled only in one case with GLUT3 antibody. Cytotrophoblast cells were only stained with antibodies against GLUT1 and GLUT3. Antibodies against GLUT4 only reacted with fibroblasts in the membranes. On amnion epithelial cells, weak immunoreactivity with insulin receptor antibodies was detected only at the electron microscopic level. The data indicate: (1) GLUT1 is located on all cells of the amnion, whereas GLUT3 is present in detectable amounts only on amnion epithelial cells and cytotrophoblast; (2) GLUT1 and GLUT3 on amnion epithelial cells are predominantly located on the apical surface; (3) GLUT4 and insulin receptors are not regularly expressed. We suggest that amnion epithelial cells cover their basal glucose requirements from the amniotic fluid and not from the maternal circulation.

Amnion↗
PubMed1993

Immunohistochemical evidence for the heterogeneity of maternal and fetal vascular endothelial cells in human full-term placenta.

The heterogeneity of endothelial cell surface antigen expression was studied in 5 human full-term placentae by means of indirect immunohistochemistry using 9 monoclonal antibodies and by staining with fluorescent-conjugated Ulex europaeus lectin, both of which are widely used endothelial cell markers. (1) A highly specific, homogeneous staining of fetal and maternal placental vessels of all sizes and anatomical regions was observed by the monoclonal antibodies PAL-E, QBEND10 and 1F10. These antibodies were even more specific than Ulex europaeus lectin, factor VIII antibody and von Willebrand factor antibody, which cross-reacted with some non-endothelial cells and structures. The reactivity of PAL-E, QBEND10 and 1F10 with residual surface cells of the basal plate strongly suggests an endothelial origin of these cells. (2) In contrast to other organs, PAL-E, QBEND10 and HM15/3 strongly stained endothelial cells of the macrovascular system in the human placenta. This might indicate an organ-associated heterogeneity of fetal endothelial cells. (3) Monoclonal antibodies against receptors for transferrin and IgG (Fc gamma RII) labeled the endothelial cells of fetal placental vessels with increasing intensity distal to the insertion of the umbilical cord. The vessels of the umbilical cord itself were unreactive. This might suggest a heterogeneity of macro- and microvascular endothelial cells.

Antibodies, Monoclonal↗
PubMed1993

Structure and dynamics of peptide-polynucleotide complexes.

The mode and the dynamics of LysTrpLys-binding to double helical DNA and to single stranded poly(A) has been analyzed by measurements of the chemical relaxation detected by fluorescence and of the rotational diffusion using the electric dichroism. The chemical relaxation, induced by electric field pulses, requires two exponentials for a satisfactory representation, indicating a two step reaction mechanism. The data are consistent with a bimolecular reaction step followed by a relatively slow intramolecular transition, which is expected to reflect "insertion" of the Trp-indole residues between the nucleic acid bases. The experimental data are analyzed quantitatively by global fitting with exact correction of the convolution due to the experimental device. In this procedure a complete set of relaxation curves is fitted directly to the reaction model and, thus artifacts resulting from erroneous assignments of coupled modes are avoided. According to this analysis the bimolecular reaction step is controlled by diffusion. The intramolecular transition in adenylate chains is found to be dependent on the chain length and on the ionic strength I: at I = 2.5 mM the "insertion" rate constant is 3 x 10(4) s-1 for the polymer and 2 x 10(5) s-1 for A(pA)19; the rate constant for poly(A) increases with increasing salt concentration. The corresponding "insertion" rate constant for DNA double helices with 30 kbp is 2.5 x 10(4) s-1. For DNA double helices we find again an increase of the "insertion" rate with increasing salt concentration and with decreasing chain length. The mode of LysTrpLys-binding to double helical DNA is compared with that of LysTyrLys, LysLeuLys and LysGlyLys by measurements of the rotational diffusion of complexes with restriction fragments of different chain lengths. The persistence lengths derived from these measurements do not reveal any special effects resulting from insertion of aromatic residues. Apparently "insertion" of indole rings into double helical DNA does not increase the length of the double helix, which may be attributed to a special form of insertion, e.g. partial insertion. According to these results the interaction of the indole residues of LysTrpLys with DNA double helices is not equivalent to e.g. intercalation of aromatic residues like ethidium-neither with respect to structure nor to dynamics.

Amino Acid Sequence↗
PubMed1992

Insulin binding to erythrocytes of nonpregnant women: a reevaluation, underlining the importance of body weights even in nonobese subjects.

Insulin binding to erythrocytes was measured in 18 healthy, non-obese women in the follicular phase and in 6 women in the mid-luteal phase of the same menstrual cycle. The presence of 55 nM and 220 nM monoclonal anti-IGF I receptor antibody (alpha-IR3) reduced only the number of low affinity binding sites for insulin by 20% and 33%, respectively. Women with relative body weights 110-119% had a lower number of high affinity receptors and an increased high affinity compared to women with relative body weights 91-109%. In women with relative body weights greater than or equal to 100%, maximum specific binding and high affinity constants increased and the receptor numbers decreased from the follicular to the luteal phase, whereas in women with relative body weights less than 100% the parameter changes were reverted. The data indicate: (1) erythrocytes contain two different classes of binding sites for insulin, (2) IGF I receptors might contribute to low-affinity binding of insulin to erythrocytes and (3) the relative body weight must be considered even for 'non-obese' control groups used in insulin binding studies of various clinical conditions.

Adult↗
PubMed1992

Insulin binding to trophoblast plasma membranes and placental glycogen content in well-controlled gestational diabetic women treated with diet or insulin, in well-controlled overt diabetic patients and in healthy control subjects.

Insulin binding to trophoblast plasma membranes and the placental glycogen content were measured in twelve healthy women, in eleven well-controlled gestational diabetic women who were treated either with diet alone (n = 4) or with insulin (n = 7) and in 18 women with well-controlled overt diabetes mellitus (six White B; four White C; eight White D). The competitive binding assay was carried out with 22 concentrations of unlabelled insulin. Binding data were analysed by a non-linear direct model fitting procedure assuming one non-cooperative binding site. Maximum specific binding was unchanged in the total collective of gestational diabetic women, but was decreased by 30% in those treated with diet (6.2 +/- 2.2%) and increased by 90% in insulin-treated women (16.4 +/- 10.2%) as compared to the control subjects (8.7 +/- 2.5%). The diet-treated women had only 40% as many and those treated with insulin had more than twice as many receptors compared to control subjects on a per mg protein basis and if expressed per total placenta. In patients with overt diabetes mellitus maximum specific binding (18.5 +/- 10.6%) was higher (p less than 0.05) due to more receptors compared to control subjects but was similar to the insulin-treated gestational diabetic patients. Maximum specific binding and receptor concentrations did not correlate linearly with maternal plasma insulin levels. Receptor affinities were virtually similar in all groups (1.8 x 10(9) l/mol). The placental glycogen content was reduced (p less than 0.05) to about 80% of that of control subjects in the diet-treated collective, whereas it was unchanged compared to control subjects in the insulin-treated gestational diabetic women despite a 40% increase (p less than 0.001) of the maternal-to-cord serum glucose ratio. In overt diabetic patients the maternal-to-cord serum glucose ratio and the placental glycogen content were higher (p less than 0.05) than in the control subjects. We conclude that trophoblast plasma membranes from gestational diabetic women treated with diet alone express less and those from women treated with insulin express more insulin receptors than those from a healthy control group in vitro. These differences could not have been disclosed without consideration of the mode of treatment. Trophoblast plasma membranes from overt diabetic women have more insulin receptors than those from healthy control subjects.

Adult↗
PubMed1991

Prolonged administration in vivo of alpha and beta adrenergic agonists decreases insulin binding to rat myocardial membranes in vitro by different mechanisms.

Male Sprague Dawley rats were continuously treated in vivo for 6, 12 and 20 hours with a combination of an alpha- (beta-) adrenoreceptor agonist and a beta- (alpha-) adrenoreceptor antagonist in subcutaneously implanted depot tablets. Crude membranes prepared from myocardial cells exhibited a decreased maximum binding of [125I]-insulin after 20 hours irrespective of the treatment applied. Scatchard and non-linear regression analysis of the displacement curves assuming two non-cooperative binding sites revealed a downregulation of the high affinity receptors for about 85% and a concomitant 2.5-fold increased receptor affinity under beta-adrenergic influence. In contrast, alpha-adrenergic treatment did not affect the receptor number but decreased the high affinity by 70%. The low affinity binding sites were virtually unaffected by the different treatments. The phospholipid and cholesterol contents of the membranes were not significantly altered. The phospholipid/cholesterol ratios after 12 and 20 hours of alpha-adrenergic treatment, however, were decreased. We suggest that the decreased binding activity of insulin receptors on rat myocardial membranes after continuous in vivo treatment with alpha- and beta- adrenergic agonists is mediated by different mechanisms.

Adrenergic alpha-Agonists↗