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At least 469 records · Page 26Linked to original sources
PubMed1975

Effects of two estradiol antagonists upon the estradiol uptake in the rat brain and peripheral tissues.

Two estradiol antagonists, Parke-Davis CI 628 and CI 680, were studied for their inhibitory potency against labeled estradiol uptake within the hypothalamus, cerebral cortex, pituitary and uterus of the ovariectomized rat. Both drugs, tested from 15 min to 24 h prior to estradiol, induced a fast and long-lasting decrease of the hormone uptake. Three degrees of inhibition were observed depending on the tissue studied: (a) the most important inhibition concerned uterus and pituitary, where the estradiol uptake was prevented by up to 90% by the largest doses of antagonists used (6.3 and 6.1 mg, respectively, for CI 268 and CI 680); (b) in the hypothalamus, the estradiol uptake was counteracted to a lower degree; the inhibition being 39% for anterior hypothalamus and 22% for medial posterior hypothalamus; (c) cerebral cortex uptake was completely unaffected by pretreatments with the antagonists. After subcellular fractionation it was observed that the nuclear uptake of estradiol was completely abolished in both hypophyseal and hypothalamic tissues if the hormonal injection was preceded by the administration of 6.3 mg of CI 628.

Animals↗
PubMed1982

Distribution of nervous system-specific forms of enolase in peripheral tissues.

The distribution of 3 forms of rat enolase (alpha alpha, alpha gamma and gamma gamma forms), including nervous system-specific forms (alpha gamma and gamma gamma), was determined in various tissues with a sensitive enzyme immunoassay system. The brain and spinal cord contained more than 100 pmol/mg protein of the alpha alpha, alpha gamma and gamma gamma enolases. Organs such as the lungs, heart, spleen, liver, and kidney contained similarly high levels of alpha alpha enolase, but these tissues contained alpha gamma and gamma gamma enolases at levels less than 1% of the central nervous tissues. High levels of the alpha gamma (greater than 10 pmol/mg) and the gamma gamma (greater than 1.5 pmol/mg) forms were found in rectum, bladder, and uterus. In gut, major portions of the nervous system-specific forms were localized in the muscle layers. Skeletal muscle and diaphragm, which are composed of striated muscle, contained low levels of 3 forms of enolase. Megakaryocytes separated from the suspension of bone marrow contained 11.3, and 0.53 amol/cell of the alpha alpha and gamma gamma enolases, respectively, with little, if any, of the alpha gamma form.

Animals↗
PubMed1980

Receptor binding interactions of the angiotensin II antagonist, 125I-[sarcosine1,leucine8]angiotensin II, with mammalian brain and peripheral tissues.

Sarcosine1,leucine8-angiotensin II ([Sar1,Leu8]AII), an angiotensin II antagonist, binds saturably, reversibly and with high affinity (KD's of 0.03-22 nM) to calf cerebellar cortex, bovine adrenal cortex and rabbit uterine membranes. The peptide specificity of 125I[Sar1,Leu8]AII binding to brain, adrenal cortex and uterus is consistent with the labeling of physiologically relevant angiotensin receptors. A detailed study of the binding potencies of 28 angiotensin peptide analogues reveals: (1) very significant correlations between peptide binding potencies at 125I-AII compared to 125I-[Sar1,Leu8]AII binding sites, (2) many similarities between brain and uterine receptor sites and marked differences between these two tissue receptors compared to adrenal cortical receptor sites, and (3) correlations among peptide physiological potencies (AII-contracted rabbit aortic strip) and receptor binding potencies in all three tissues labeled with either 125I-AII or 125I-[Sar1,Leu8]AII. The correlations are much better for adrenal cortex than for brain or uterus, suggesting that adrenal cortical angiotensin receptors are similar to aorta angiotensin receptors.

Adrenal Cortex↗
PubMed1995

Expression of the mouse and rat mas proto-oncogene in the brain and peripheral tissues.

We isolated the mas proto-oncogene from a mouse genomic library. Sequence analysis showed that it contains an open reading frame without intervening sequences. The amino acid sequence deduced confirms the seven-transmembrane-domain structure and exhibits 97% and 91% amino acid homology with the rat and the human Mas, respectively. In mice and rats, mas mRNA was detected in the testis, kidney, heart, and in the brain regions: hippocampus, forebrain, piriform cortex, and olfactory bulb. Testicular mas mRNA from rats increases markedly during development, while cerebellar mRNA is high postnatally but completely disappears at later stages. We conclude that the product of the mouse mas gene may be involved in the development of the brain and testis.

Amino Acid Sequence↗
PubMed1983

Aromatization of steroids in peripheral tissues.

The action of glucocorticoids on aromatase activity in human adipose tissue has been investigated. Oestrogen production was increased in tissue maintained in the presence of dexamethasone and cortisol. Dexamethasone was effective at concentrations as low as 1 nmol/l. In contrast, over the 40 h incubation period, cortisol was only effective at concentrations in excess of 500 nmol/l, although after conditions of prolonged incubation, induction of aromatase activity was measurable using cortisol concentrations as low as 28 nmol/l. There were apparent variations in both basal levels of aromatic activity and in response to glucocorticoids in adipose tissue taken from various sites within the body.

Adipose Tissue↗
PubMed1985

Production and metabolism of dihydrotestosterone in peripheral tissues.

The production and metabolism of dihydrotestosterone (DHT) was studied in 10 normal men using constant infusions of [7-3H]-delta 4 -androstenedione (A)/[4-14C]DHT (6 men) or of [7-3H]testosterone (T)/[4-14C]DHT (4 men) with measurement of radioactivity as precursor and product in the brachial artery, and a superficial vein (draining primarily adipose tissue) and deep vein (draining primarily muscle) in the arm opposite to the infusion. The metabolic clearance rates (MCR) were (mean +/- SE) 560 +/- 55, 1620 +/- 80, and 790 +/- 65, 1/day for DHT, A and T respectively. The overall conversions (percent of A or T infused which was measured as DHT in arterial blood) were 2.3 +/- 0.8% and 2.7 +/- 0.5% for A to DHT and T to DHT. Of the DHT entering the adipose tissue 13.8 +/- 3.4% was metabolized and of that entering muscle 5.8 +/- 1.8% was metabolized. On the basis of assumed blood flows, adipose tissue and muscle metabolism each carry out approx. 7-8% of the overall metabolism of DHT. Of the A entering the forearm adipose tissue 1.9 +/- 0.5% was converted to DHT. Extrapolated to the body's adipose tissue, this represents 14% of the total A converted to DHT. Of the T entering the forearm adipose tissue 1.2 +/- 0.3% was converted to DHT. Extrapolated to the body's adipose tissue, this represents 6% of the total T converted to DHT. In three out of six subjects infused with A/DHT and in three out of four subjects infused with T/DHT small gradients indicating conversion of A and T to DHT by tissues drained by the deep vein were found. The mean value for the conversion of A to DHT across the deep vein tissues was 0.84 +/- 0.51% and for T to DHT was 0.28 +/- 0.12%. Both adipose tissue and muscle metabolize DHT but only adipose tissue appears to play a role in the conversion of A and T to DHT.

Adipose Tissue↗