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PubMed1991

Nitric oxide synthase and neuronal NADPH diaphorase are identical in brain and peripheral tissues.

NADPH diaphorase staining neurons, uniquely resistant to toxic insults and neurodegenerative disorders, have been colocalized with neurons in the brain and peripheral tissue containing nitric oxide synthase (EC 1.14.23.-), which generates nitric oxide (NO), a recently identified neuronal messenger molecule. In the corpus striatum and cerebral cortex, NO synthase immunoreactivity and NADPH diaphorase staining are colocalized in medium to large aspiny neurons. These same neurons colocalize with somatostatin and neuropeptide Y immunoreactivity. NO synthase immunoreactivity and NADPH diaphorase staining are colocalized in the pedunculopontine nucleus with choline acetyltransferase-containing cells and are also colocalized in amacrine cells of the inner nuclear layer and ganglion cells of the retina, myenteric plexus neurons of the intestine, and ganglion cells of the adrenal medulla. Transfection of human kidney cells with NO synthase cDNA elicits NADPH diaphorase staining. The ratio of NO synthase to NADPH diaphorase staining in the transfected cells is the same as in neurons, indicating that NO synthase fully accounts for observed NADPH staining. The identity of neuronal NO synthase and NADPH diaphorase suggests a role for NO in modulating neurotoxicity.

Adrenal Medulla↗
PubMed1988

Anatomical distribution of vasoactive intestinal peptide binding sites in peripheral tissues investigated by in vitro autoradiography.

Vasoactive intestinal polypeptide has a widespread distribution in the body, occurring in both the central and peripheral nervous systems and considerable information is available on its distribution, physiology, and pharmacological actions. Receptors for VIP have been demonstrated previously in peripheral tissues by conventional binding techniques using isolated membrane preparations. However, information on their precise localization is limited. We therefore localized binding sites in a variety of guinea pig and rat tissues by in vitro autoradiography and made a parallel study of the distribution of VIP nerves in these tissues using immunocytochemistry. [125I]VIP was prepared by the chloramine T method and shown to be pharmacologically active. After a preincubation procedure to remove endogenously bound VIP, unfixed cryostat sections were incubated with 1 nM [125I]VIP. To determine specific binding, sections were incubated in the presence or absence of 1 microM unlabeled VIP. Autoradiograms were generated by exposing the sections to LKB-Ultrofilm or emulsion-coated coverslips. Dense binding occurred in discrete locations within the gastrointestinal, respiratory, and genital tracts, correlating with known actions of VIP and, to various extents, with the distribution of VIP nerves. For example, there was precise localization to respiratory epithelium, smooth muscle of airways and blood vessels, and alveolar walls, in keeping with the effects of VIP on vascular and airway smooth muscle and mucus secretion.

Animals↗
PubMed2004

Crystal structures of the multispecific 17beta-hydroxysteroid dehydrogenase type 5: critical androgen regulation in human peripheral tissues.

Human type 5 17beta-hydroxysteroid dehydrogenase (17beta-HSD5;AKR1C3) plays a major role in the metabolism of androgens in peripheral tissues. In prostate basal cells, this enzyme is involved in the transformation of dehydroepiandrosterone into dihydrotestosterone, the most potent androgen. It is thus a potential target for prostate cancer therapy because it is understood that the testosterone formation by this enzyme is an important factor, particularly in patients who have undergone surgical or medical castration. Here we report the first structure of a human type 5 17beta-HSD in two ternary complexes, in which we found that the androstenedione molecule has a different binding position from that of testosterone. The two testosterone-binding orientations in the substrate-binding site demonstrate the structural basis of the alternative binding and multispecificity of the enzyme. Phe306 and Trp227 are the key residues involved in ligand recognition as well as product release. A safety belt in the cofactor-binding site enhances nicotinamide adenine dinucleotide phosphate binding and accounts for its high affinity as demonstrated by kinetic studies. These structures have provided a dynamic view of the enzyme reaction converting androstenedione to testosterone as well as valuable information for the development of potent enzyme inhibitors.

17-Hydroxysteroid Dehydrogenases↗
PubMed1992

The influence of different levels of PEEP on peripheral tissue perfusion measured by subcutaneous and transcutaneous oxygen tension.

OBJECTIVE: To compare subcutaneous (PscO2) and transcutaneous (PtcO2) oxygen tension measurements in relation to hemodynamic variables at different levels of PEEP, and to evaluate the usefulness of these measurements as monitors of peripheral tissue perfusion. DESIGN: Prospective trial. SETTING: Intensive care unit in a university hospital. PATIENTS: Seven patients with gastric cancer who where undergoing total gastrectomy. INTERVENTIONS: Silicone catheter was placed in the upper arm and transcutaneous oxygen monitor was placed on the upper part of the chest. A pulmonary artery catheter was placed in the right pulmonary artery. MEASUREMENTS AND RESULTS: PscO2 and PtcO2 together with hemodynamic variables were measured at different levels of PEEP. Progressive increase of PEEP reduced cardiac index (CI) (p < 0.05) with a concomitant decrease of PscO2 (p < 0.05) and oxygen delivery (DO2) (p < 0.05). Changes in PtcO2 paralleled changes in arterial oxygen tension (PaO2), but no correlation was found between PtcO2, CI and DO2. CONCLUSION: PscO2 is a sensitive indicator of subcutaneous tissue perfusion, which can be used to identify the PEEP level, with optimum peripheral perfusion. PscO2 seems to be a more reliable indicator of tissue perfusion than PtcO2.

Aged↗
PubMed1997

Distribution of myomodulin-like and buccalin-like immunoreactivities in the central nervous system and peripheral tissues of the mollusc, Clione limacina.

The distribution of the myomodulin-like and buccalin-like immunoreactivities in the central nervous system and peripheral tissues associated with feeding was examined in the pteropod mollusc Clione limacina by using wholemount immunohistochemical techniques. Immunoreactive neurons and cell clusters were located in all central ganglia except the pleural ganglia, with approximately 50 central neurons reactive to myomodulin antiserum and 60 central neurons reactive to buccalin antiserum. All central ganglia contained a dense network of myomodulin- and buccalin-immunoreactive processes in their neuropil regions and connectives. In the periphery, the primary attention was focused on the tissues associated with feeding, especially feeding structures unique to Clione, such as hook sacs and buccal cones, which are used for prey capture and acquisition. All of these feeding structures contained myomodulin-immunoreactive and buccalin-immunoreactive fibers, with each peptide family showing specific innervation fields that were common in buccal cones and were totally different in the hook sacs. The specific central and peripheral distribution of myomodulin-like and buccalin-like immunoreactivities as well as specific effects of the exogenous peptides on identified neurons involved in the control of feeding behavior and swimming suggest that neuropeptides from myomodulin and buccalin families act as neurotransmitters or neuromodulators in a variety of central circuits and in the peripheral neuromuscular systems associated with feeding in Clione limacina.

Animals↗
PubMed2002

Distribution of neuropeptide Y Y1 receptors in rodent peripheral tissues.

Using a sensitive immunohistochemical technique, the localization of neuropeptide Y (NPY) Y1-receptor (Y1R)-like immunoreactivity (LI) was studied in various peripheral tissues of rat. Wild-type (WT) and Y1R-knockout (KO) mice were also analyzed. Y1R-LI was found in small arteries and arterioles in many tissues, with particularly high levels in the thyroid and parathyroid glands. In the thyroid gland, Y1R-LI was seen in blood vessel walls lacking alpha-smooth muscle actin, i.e., perhaps in endothelial cells of capillaries. Larger arteries lacked detectable Y1R-LI. A distinct Y1R-immunoreactive (IR) reticulum was seen in the WT mouse spleen, but not in Y1R-KO mouse or rat. In the gastrointestinal tract, Y1R-positive neurons were observed in the myenteric plexus, and a few enteroendocrine cells were Y1R-IR. Some cells in islets of Langerhans in the pancreas were Y1R-positive, and double immunostaining showed coexistence with somatostatin in D-cells. In the urogenital tract, Y1R-LI was observed in the collecting tubule cells of the renal papillae and in some epithelial cells of the seminal vesicle. Some chromaffin cells of adrenal medulla were positive for Y1R. The problem of the specificity of the Y1R-LI is evaluated using adsorption tests as well as comparisons among rat, WT mouse, and mouse with deleted Y1R. Our findings support many earlier studies based on other methodologies, showing that Y1Rs on smooth muscle cells of blood vessels mediate NPY-induced vasoconstriction in various organs. In addition, Y1Rs in other cells in parenchymal tissues of several organs suggest nonvascular effects of NPY via the Y1R.

Animals↗
PubMed1991

Distribution of neurokinin A-like and neurokinin B-like immunoreactivity in human peripheral tissues.

Using specific radioimmunoassay and immunocytochemistry for neurokinin A (NKA) and neurokinin B (NKB), distribution and localization of the two peptides in human peripheral tissues were studied. Both NKA-like immunoreactivity (NKA-LI) and NKB-like immunoreactivity (NKB-LI) were present in the walls of the gut and gall bladder and in the pancreas. In the gut, the values for NKA-LI were 0.56-35.73 pmol/g wet weight, while those in pancreas and gall bladder were 0.64-0.68 and 0.36 pmol/g wet weight, respectively. The values of NKB-LI were 0.45-2.66 pmol/g wet weight in the gut, 0.93-1.65 pmol/g wet weight in the pancreas, and 0.30 pmol/g wet weight in the gall bladder. The immunocytochemical reactivity to both peptides was localized to ganglia of the submucosal and myenteric nerve plexuses in the gut wall, and to neurons in the muscle layer and mucosa of the gut wall. Weak but positive NKA-LI appeared in nerve cells of the pancreas, while NKB-LI was not detectable in the pancreas. Conversely, in the gall bladder wall, NKA-LI was undetectable while a very faint NKB-LI was found in the muscle layer. The localization of NKA corresponded closely to that of NKB in the tissues although the relative concentrations of the peptides varied from organ to organ.

Digestive System↗
PubMed1989

Sex-dependent and sex-independent distribution of the beta-subunit of nerve growth factor in the central nervous and peripheral tissues of mice.

Levels of the beta-subunit of nerve growth factor (beta-NGF) were measured in the central nervous and peripheral tissues of mice using a highly sensitive, sandwich-type enzyme immunoassay system. Antiserum was raised in rabbits against the 7S form of NGF, which was purified from mouse submandibular glands. beta-NGF-specific antibody isolated on a column of Sepharose CL-4B coupled with purified beta-NGF reacted only with beta-NGF. The assay for beta-NGF was performed by incubation of F(ab')2 fragments of the antibody immobilized on a polystyrene ball with tissue extract and then with the same antibody Fab' fragments labeled with beta-D-galactosidase, followed by measurement of galactosidase activity. Our assay system was found to be highly sensitive (minimal detection limit, 0.3 pg/0.3 ml of assay mixture). Furthermore, the presence of gelatin hydrolysates and protease inhibitors during preparation of tissue extracts enabled us to determine the precise levels of beta-NGF in almost all organs of mice. The amount of beta-NGF in submandibular glands was extremely high, and its level increased rapidly until mice were 2 months of age; then, the level continued to increase slowly until mice were 1 year old (3-5 mg/g of tissue). In serum, some of the 2-month-old males, but none of the females, exhibited a fairly high level of beta-NGF (greater than 100 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1978

Abnormalities of triiodothyronine binding to lymphocyte and fibroblast nuclei from a patient with peripheral tissue resistance to thyroid hormone action.

T3 binding to lymphocyte nuclei has been studied in normal individuals and in a patient (MaG) with peripheral resistance to thyroid hormone action. This syndrome is defined by the presence of hypothyroidism or euthyroidism with high plasma levels of thyroid hormone. T3 bound to a single set of binding sites in normal adult lymphocyte nuclei with a mean Ka of 8.9 +/- 7.1 x 109 M-1, and a capacity of 4.4 +/- 2.9 fmol/100 micrograms DNA. A single binding site was also disclosed in MaG's lymphocytes with a Ka of 0.43 x 109 M-1 and a capacity of 10.5 fmol/100 micrograms DNA. This low affinity was not due to the presence of high plasma T3 level in the patient, since administration of 100 micrograms T3 to normal adult volunteers induced the presence of two different binding sites. The mechanism responsible for this phenomenon is unknown. To binding was also studied using cultured fibroblasts which were incubated in serum-less medium before the binding experiments. One single binding site (Ka, 1.9 x 10(10) M-1, capacity, 12.9 fmol/100 micrograms DNA) was detected in normal fibroblast nuclei. In contrast, a curvilinear Scatchard plot was obtained when MaG's fibroblasts were used. This result could be compatible with the presence of either two different binding sites or negative cooperativity. In support of the latter possibility, Hill plots gave a number lower than unity. The results suggest that the syndrome of peripheral tissue resistance to thyroid hormone action due to a defect at the level of the nuclear receptor. The possible existence of similar syndromes due to an alteration at the level of a post-T3-binding mechanism is not eliminated.

Adolescent↗
PubMed1991

[Creatine phosphokinase isoenzymes (CK BB) of the brain in peripheral tissues in schizophrenia].

The activity and content of the brain isoenzyme of creatine phosphokinase-BB (CPK-BB) were investigated in the peripheral tissues containing this isoenzyme (in the small intestine and heart) in health and schizophrenia. The decrease of CPK-BB activity and content in schizophrenic brain was shown before. The present work demonstrates the reduction of CPK-BB activity and concentration not only in the brain of mental patients but also in the intestine and heart tissues. A high correlation was discovered between the CPK-BB level in the brain and in the intestine of schizophrenic patients (r = 0.85).

Brain↗
PubMed2000

Ts65Dn mouse, a Down syndrome model, exhibits elevated myo-inositol in selected brain regions and peripheral tissues.

myo-Inositol is elevated in the Down syndrome (DS; trisomy 21) brain and may play a role in mental retardation. In the present study, we examined brain regions and peripheral tissues of Ts65Dn mouse, a recently characterized genetic model of DS, for abnormal myo-inositol accumulation. A GC/MS technique was used to quantitate myo-inositol and other polyol species (ribitol, arabitol, xylitol, and 1,5-anhydrosorbitol) in tissues from the Ts65Dn mice and control diploid mice. myo-Inositol was found to be elevated in frontal cortex, hippocampus, and brain stem but not in cerebellum of the Ts65Dn mouse. Among peripheral organs examined, liver and skeletal muscle were found to excessively accumulate myo-inositol. In all tissues, concentrations of polyol internal controls were normal. The Ts65Dn mouse is useful to study the possible effect of elevated myo-inositol on cellular processes.

Animals↗
PubMed1983

Augmented vasoconstrictor response to head-up tilt in peripheral tissues during beta-receptor blockade.

Subcutaneous and skeletal muscle blood flow in the forearm during 30 degrees head-up tilt was studied in 15 healthy subjects before and during treatment with propranolol. Relative blood flow was estimated by the local 133Xe washout technique. Head-up tilt elicited greater vasoconstriction in both tissues during beta-receptor blockade as compared to the pretreatment period. Proximal nerve blockade with lidocaine prevented the vasoconstrictor response in subcutaneous tissue to the tilt. In skeletal muscle injection of a low dose of propranolol had no effect on the vasoconstrictor response to tilt. Therefore, the augmented vasoconstrictor response to head-up tilt during beta-receptor blockade is most probably due to centrally elicited (baroreceptor) and neurogenically mediated impulses to resistance vessels in peripheral tissues and not to "unmasking" of peripheral alpha-receptors.

Adrenergic beta-Antagonists↗
PubMed1993

Effect of guanine nucleotides and temperature on calcitonin gene-related peptide receptor binding sites in brain and peripheral tissues.

Recent data have suggested the existence of at least two major classes of calcitonin gene-related peptide (CGRP) receptors in brain and peripheral tissues [Henke et al., Brain Res., 410 (1987) 404-408; Dennis et al., J. Pharmacol. Exp. Ther., 251 (1989) 718-725; ibid, 254 (1990) 123-128; Quirion et al., Ann. NY Acad. Sci., 657 (1992) 88-105]. However, little is currently known in the structure characteristics of CGRP receptors as cloning as yet to be reported. In the present study, the sensitivity of [125I]humanCGRP alpha binding to guanine nucleotides and temperature was investigated in guinea pig atria (prototypical CGRP1 tissue) guinea pig vas deferens (prototypical CGRP2 tissue) and in the rat brain and cerebellum (mixed assay). Binding isotherms of [125I]hCGRP alpha in those four tissue preparations were curvilinear and best fitted to a two-site model under most assay conditions. The high affinity binding component was highly temperature-sensitive and accounted, under experimental conditions, for up to 18% of the total population of receptors. Moreover, these high affinity sites were also highly sensitive to guanine nucleotides (Gpp(NH)p, 100 microM) in all preparations although to a different extend depending upon assay temperatures. Taken together, this suggests that the different CGRP receptor subtypes present in these tissue all belong to a G-protein coupled receptor family.

Animals↗
PubMed2001

[Glutamate receptors and transporters in the brain and peripheral tissues].

Functional diversity of glutamate receptors in the central nervous system (CNS) is a consequence of their considerable molecular diversity. The family of glutamate receptors including their subunits consists of more than 25 proteins. It is the result of gene expression as well as extensive post-transcriptional modifications. Evidence is increasing that glutamate receptors are localised not only in the CNS, but also in the peripheral tissues. Whereas characteristics and physiological significance of peripheral glutamate receptors are little understood, there are studies indicating their role in hormone secretion, neuromuscular functions, sensory transmission and paracrine signalization. In addition, peripheral glutamate receptors may participate in mediating of excitatory amino acids toxicity. A special attention is paid to glutamate receptors localised in the heart and adrenals, as these receptors may be involved in the maintenance of homeostatic mechanisms under pathological or stress conditions.

Adrenal Glands↗
PubMed2006

Photoperiodic regulation of PER1 and PER2 protein expression in rat peripheral tissues.

Circadian oscillations in biological variables in mammals are controlled by a central pacemaker in the suprachiasmatic nuclei (SCN) of the hypothalamus which coordinates circadian oscillators in peripheral tissues. The molecular clockwork responsible for this rhythmicity consists of several clock genes and their corresponding proteins that compose interactive feedback loops. In the SCN, two of the genes, Per1 and Per2, show circadian rhythmicity in their expression and protein production. This SCN rhythmicity is modified by the length of daylight, i.e. the photoperiod. The aim of the present study was to find out whether profiles of PER1 and PER2 proteins in peripheral organs are also affected by the photoperiod. Rats were maintained under a long photoperiod with 16 h of light and 8 h of darkness per day (LD 16:8) and under a short, LD 8:16, photoperiod. The PER1 and PER2 daily profiles were measured in peripheral organs by Western blotting. The photoperiod affected significantly the PER1 profile in livers and the PER2 profile in lungs and hearts. In lungs, PER2 in the cytoplasmic, but not in the nuclear fraction, was affected significantly. The effect of the photoperiod on PER1 profiles in peripheral organs appears to differ from that in the SCN.

Animals↗
PubMed1986

Binding profile of a novel cardioselective muscarine receptor antagonist, AF-DX 116, to membranes of peripheral tissues and brain in the rat.

The heterogeneity of muscarine receptors was examined in two brain regions (cerebral cortex and cerebellum) and in some parasympathetically innervated peripheral tissues (heart, salivary gland and intraorbital lacrimal gland), by in vitro binding techniques. As a tool, we used a new antimuscarinic compound, AF-DX 116 (see text for structural formula and chemical name). In competition experiments against 3H-N-methylscopolamine (3H-NMS) or 3H-pirenzepine (3H-PZ), AF-DX 116 was found to bind with high affinity to muscarine receptors in the heart and cerebellum (KD's approximately equal to 115 nM), with intermediate affinity to M1 receptors in neuronal tissue (KD = 760 nM) and with low affinity to receptors in exocrine glands (KD's approximately equal to 3200 nM). Its receptor interaction was found to be of the simple, competitive type. Thus, AF-DX 116 shows a novel cardioselective profile. On the basis of the results which demonstrate that the muscarine receptors in the heart and exocrine glands are clearly distinct, it is proposed that these receptors may be subclassified as M2 cardiac type and M2 glandular type muscarine receptors.

Animals↗
PubMed1992

The relation between triglyceride synthesis in peripheral tissues and postprandial plasma triglyceride levels: preliminary evidence of a role for acylation stimulating protein.

The present study examines the hypothesis that the rate at which peripheral tissues synthesize triglycerides is a key determinant of the rate at which they are removed from plasma. The cells of greatest interest in this regard would, of course, be the adipocytes. However, serial sampling of this tissue is not possible in man. We have approached the question indirectly, by studying triglyceride synthesis in human mononuclear cells before and after an oral fat load. In addition, plasma levels of Acylation Stimulating Protein (ASP) were measured after an overnight fast and 4 h after ingestion of the oral fat load. Similar measurements were made in the same subjects after fasting overnight and with the fast extended for 4 additional hours. With the extended fast, no parameter measured changed significantly. However, after the oral fat load, the following changes were found to be significant: plasma triglycerides increased (63.6 +/- 31.1 vs 101.5 +/- 43 mg/dl, p less than 0.005) as did d less than 1.006 g/ml triglycerides (42.3 +/- 22.8 vs 78.0 +/- 39.7 mg/dl, p less than 0.005) and plasma ASP (10.4 +/- 2.2 vs 14.7 +/- 2.3 mg/dl, p less than 0.005). In addition, the rate of triglyceride synthesis in the mononuclear cells increased significantly (1.22 +/- 0.3 vs 1.52 +/- 0.3 nmol oleate/mg cell protein per h, p less than 0.005). There was also a significant inverse relation between the increase in the d less than 1.006 triglycerides between 0 and 4 h and the increase in triglyceride synthesis in the mononuclear cells (r = 0.91, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Acylation↗
PubMed1998

Effects of acute administration of L-arginine on morphine antinociception and morphine distribution in central and peripheral tissues of mice.

The effect of acute treatment with L-arginine, a substrate for nitric oxide synthase (NOS) that forms NO, an important second messenger, on morphine antinociception and distribution of morphine in central and peripheral tissues of male Swiss-Webster mice was determined. The antinociception activity of morphine (10 mg/kg, s.c.) was attenuated by 400 and 800 mg/kg doses of L-arginine, but a lower dose (200 mg/kg) had no effect. D-Arginine (200-800 mg/kg) did not modify morphine antinociception. The dose of L-arginine (200 mg/kg) that did not modify morphine antinociception also did not alter the distribution of morphine in brain regions and spinal cord. A dose of 800 mg/kg of L-arginine produced a significant decrease in the concentration of morphine in midbrain and spinal cord. The highest dose of L-arginine (800 mg/kg) also increased the concentration of morphine in spleen. None of the doses of L-arginine modified the concentration of morphine in serum or urine. The results suggests that acute activation of the NO system attenuates morphine antinociception possibly by inhibiting its uptake in central sites (midbrain and spinal cord) involved in antinociceptive actions.

Analgesics, Opioid↗