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PubMed1985

Quantitation of apolipoprotein E mRNA in the liver and peripheral tissues of nonhuman primates.

A sensitive DNA-excess solution hybridization assay was used to quantitate apo-E mRNA in the liver and peripheral tissues of two nonhuman primates, Macaca fascicularis and Cercopithecus aethiops. When expressed on the basis of total RNA, apo-E mRNA values for M. fascicularis adrenal, brain, testis, and spleen ranged from 17-52% of the liver value. Apo-E mRNA values for mesenteric lymph node, kidney, thymus, and skeletal muscle were 1-5% of the liver value. When expressed on a cellular basis, apo-E mRNA was most abundant in the liver at approximately 1200 molecules/cell. Peripheral tissues showed a continuous range of apo-E mRNA from 1.5 molecules/cell in the thymus up to 350 molecules/cell in the brain. Similar results were obtained with peripheral tissues from C. aethiops in which case apo-E mRNA also was found in skin, lung, skeletal muscle, small intestine, and vascular tissues such as heart, aorta, and brachial artery. Calculation of the total apo-E mRNA/organ showed that most of the apo-E mRNA was present in the liver. However, summation of apo-E mRNA in peripheral tissues indicated that 20-40% of total body apo-E mRNA was extrahepatic. This results indicates that apo-E made in peripheral tissues may play a quantitatively important role in cholesterol metabolism since peripheral tissues have the potential to contribute a significant fraction of plasma apo-E.

Adrenal Glands↗
PubMed1991

Visceral and peripheral tissue perfusion after cardiac surgery.

Visceral and peripheral tissue perfusion and oxygenation were studied in ten patients in the early phase after coronary artery bypass grafting. Visceral perfusion was assessed indirectly, by determining gastric intramucosal pH. As parameters of peripheral tissue perfusion and oxygenation, subcutaneous tissue PO2 (PscO2), transcutaneous PO2 (PtcO2). PtcO2 index (PtcO2/PaO2), laser-Doppler skin red-cell flux (RCF) and fingertip temperature (Tft) were recorded in the upper extremity. Central haemodynamics, rectal temperature and blood gases were also measured. The inspired oxygen concentration was maintained at 30 v/v%. Gastric intramucosal pH declined progressively during the first 3 hours in the intensive care unit, reached its minimum at 5 hours and thereafter slowly increased. The peripheral vascular bed was shut down on admission to the ICU, as indicated by low values of PscO2, PtcO2, PtCO2 index, RCF and Tft. These parameters began to rise after the next 2-4 hours and peaked by the end of the 8-hour study period, indicating complete opening of the peripheral vascular bed.

Body Temperature↗
PubMed2002

Nuclear RelB+ cells are found in normal lymphoid organs and in peripheral tissue in the context of inflammation, but not under normal resting conditions.

Differentiated dendritic cells (DC) have been identified by the presence of nuclear RelB (nRelB) and HLA-DR, and the absence of CD20 or high levels of CD68, in lymph nodes and active rheumatoid arthritis synovial tissue. The current studies aimed to identify conditions in which nRelB is expressed in human tissues, by single and double immunohistochemistry of formalin-fixed peripheral and lymphoid tissue. Normal peripheral tissue did not contain nRelB+ cells. nRelB+ DC were located only in T- or B-cell areas of lymphoid tissue associated with normal organs or peripheral tissues, including tonsil, colon, spleen and thymus, or in association with T cells in inflamed peripheral tissue. Inflamed sites included skin delayed-type hypersensitivity reaction, and a wide range of tissues affected by autoimmune disease. Nuclear RelB+-HLA-DR- follicular DC were located in B-cell follicles in lymphoid organs and in lymphoid-like follicles of some tissues affected by autoimmune disease. Lymphoid tissue T-cell areas also contained nRelB(-)-HLA-DR+ cells,some of which expressed CD123 and/or CD68. Nuclear RelB+ cells are found in normal lymphoid organs and in peripheral tissue in the context of inflammation, but not under normal resting conditions.

Autoimmune Diseases↗
PubMedDate not supplied

Ineffective peripheral tissue perfusion: Clinical validation in patients with hypertensive cardiomiopathy.

PURPOSE: To validate defining characteristics of ineffective peripheral tissue perfusion using vasomotor function assessment. METHODS: Twenty-four patients with hypertensive cardiomiopathy were evaluated for 18 defining characteristics of ineffective peripheral tissue perfusion and underwent vasomotor function assessment with induction of reactive hyperemia, intra-arterial infusion of acetylcholine, and pulse wave velocity measurement. The Student's t test and Kruskall-Wallis test were used to assess the significance of relationships between defining characteristics and vasomotor function data. FINDINGS: Diminished lower extremity pulses were associated with diminished forearm blood flow during acetylcholine infusion; left ventricular overload, intermittent claudication, and diminished skin moisture were associated with elevated pulse wave velocity values. CONCLUSION: The defining characteristics of ineffective peripheral tissue perfusion were highly associated with vasomotor function data as "gold standards" for that diagnosis. PRACTICE IMPLICATIONS: Nurses should be able to accurately assess diminished lower extremity pulses, intermittent claudication, and diminished skin moisture as relevant characteristics of ineffective peripheral tissue perfusion in patients with hypertensive cardiomiopathy.

Acetylcholine↗
PubMed1989

Energy balance and diabetes. The effects of cold exposure, exercise training, and diet composition on glucose tolerance and glucose metabolism in rat peripheral tissues.

The effects of cold exposure, exercise training, and diet (high fat versus high carbohydrate) on glucose tolerance and glucose metabolism in rat peripheral tissues will be briefly reviewed. Stimulation of energy expenditure by cold exposure (4 degrees C) or exercise training generally leads to decreased plasma insulin levels and to an improvement in glucose tolerance, suggesting that insulin action on peripheral tissues is increased when energy expenditure is stimulated. On the contrary, feeding high-fat diets to sedentary rats living in the warm (25 degrees C) induces hyperinsulinemia and insulin resistance resulting in a marked deterioration of glucose tolerance. Nevertheless, cold exposure reverses the diabetogenic effects of high-fat feeding, demonstrating that nutrition-induced insulin resistance is amplified in sedentary animals living at temperatures close to thermoneutrality. Radioactive tracer studies of 2-deoxyglucose uptake in peripheral tissues revealed that cold exposure synergistically potentiates the effects of insulin on glucose uptake in skeletal muscles as well as in white and brown adipose tissues. However, more recent data showed that cold exposure improves glucose tolerance and stimulates glucose uptake in starved animals (ie., in the virtual absence of circulating insulin) nearly by the same order of magnitude as in fed animals. It is therefore concluded that cold exposure, and possibly also exercise, improve glucose tolerance and stimulate glucose uptake in peripheral tissues primarily by enhancing glucose oxidation via insulin-independent pathways, and secondarily by increasing the responsiveness of peripheral tissues to insulin.

Acclimatization↗
PubMed2004

Advances in the detection of prion protein in peripheral tissues of variant Creutzfeldt-Jakob disease patients using paraffin-embedded tissue blotting.

The accumulation of PrP(Sc), an abnormal and disease-associated form of the normal prion protein (PrP(c)), within the central nervous system (CNS) is a key pathological feature of Creutzfeldt-Jakob disease (CJD). Following limited proteolytic digestion of PrP(Sc), the detection of PrP(res) within lymphoid tissues is a unique characteristic of variant CJD in comparison with other human prion diseases, raising fears of an increased risk of iatrogenic spread. Because levels of PrP(res) in lymphoid tissues are lower than those found in CNS tissue, there is concern that other peripheral tissues may harbour infectivity at levels that current detection systems cannot demonstrate PrP(res). We have modified the paraffin-embedded tissue blot (PET blot), a technique combining immunohistochemistry (IHC), histoblot and Western blotting, for the detection of PrP(res) in paraffin sections in peripheral tissues in variant CJD. Five cases of variant CJD were examined, using a panel of anti-PrP antibodies. In each of these five cases, spleen, tonsil, lymph nodes and dorsal root ganglia showed an increase in the sensitivity and specificity of labelling using the PET blot when compared with optimized PrP(res) IHC methods. Control cases showed no evidence of PrP accumulation in either peripheral or CNS tissues. Autopsy and biopsy brain material from sporadic CJD cases also showed an increased sensitivity of PrP(res) detection with the PET blot, confirming its value as an important diagnostic and research tool in human prion diseases.

Adolescent↗
PubMed1989

Ketanserin reduces a particular monoamine pool in peripheral tissues.

The effect of ketanserin and tetrabenazine treatment on monoamine and metabolite levels in central and peripheral tissues was investigated in young and senescent male Wistar and spontaneously hypertensive Okamota rats. Control animals showed significantly higher brain monoamine levels and 3 and 5.5 times higher dopamine levels in the vas deferens of the senescent and hypertensive rats, as compared with young normotensive rats. Ketanserin (20 mg/kg) produced an average of 20% reduction of brain monoamines without changing metabolite levels. In the vas deferens, dopamine was reduced by 85% and norepinephrine by 30%. In cardiovascular tissues, norepinephrine was 40% to 50% decreased and in the spleen norepinephrine was 60% and 5-hydroxytryptamine 30% reduced. Ketanserin (5 mg/kg) had only a marked effect on dopamine in the vas deferens and on norepinephrine in the portal vein. Tetrabenazine at 20 mg/kg produced complete depletion of the monoamine and 3-methoxytyramine levels in the brain with a concomitant rise in acid metabolites. In peripheral tissues, amine levels were reduced by 55% to 80%; dopamine in the vas deferens was 93% decreased. Tetrabenazine (5 mg/kg) still had marked effects in all tissues. The drug effects were the same in the three types of rats and the effects did not markedly change with chronic treatment up to 20 days. It is hypothesized that at least two different mechanisms are involved in monoamine depletion, 1) the classically proposed inhibition of uptake of monoamines in the storage vesicles, a property of tetrabenazine not shared by ketanserin in vivo and 2) triggering of the release of monoamines from a ketanserin-sensitive pool, which is relatively more important in peripheral tissues than in the brain. The latter process is probably mediated by previously identified ketanserin-binding release sites on nerve terminals and platelets. The ketanserin-sensitive monoamine pools in peripheral tissues may have a role in cardiovascular pathologies.

Age Factors↗
PubMed2006

Absence of VLDL secretion does not affect alpha-tocopherol content in peripheral tissues.

alpha-Tocopherol is a lipid-soluble antioxidant that helps to prevent oxidative damage to cellular lipids. alpha-Tocopherol is absorbed by the intestine and is taken up and retained by the liver; it is widely presumed that alpha-tocopherol is then delivered to peripheral tissues by the secretion of VLDL. To determine whether VLDL secretion is truly important for the delivery of alpha-tocopherol to peripheral tissues, we examined alpha-tocopherol metabolism in mice that lack microsomal triglyceride transfer protein (Mttp) expression in the liver and therefore cannot secrete VLDL (Mttp(Delta/Delta) mice). Mttp(Delta/Delta) mice have low plasma lipid levels and increased stores of lipids in the liver. Similarly, alpha-tocopherol levels in the plasma were lower in Mttp(Delta/Delta) mice than in controls, whereas hepatic alpha-tocopherol stores were higher. However, alpha-tocopherol levels in the peripheral tissues of Mttp(Delta/Delta) mice were nearly identical to those of control mice, suggesting that VLDL secretion is not critical for the delivery of alpha-tocopherol to peripheral tissues. When fed a diet containing deuterated alpha-tocopherol, Mttp(Delta/Delta) and control mice had similar incorporation of deuterated alpha-tocopherol into plasma and various peripheral tissues. We conclude that the absence of VLDL secretion has little effect on the stores of alpha-tocopherol in peripheral tissues, at least in the mouse.

Animals↗
PubMed1987

Depressed progesterone accumulation by the brain and peripheral tissues of diabetic C57BL/KsJ mice: normalization by estrogen therapy.

The effects of diabetes on the uptake and incorporation of 3H-progesterone (P) in various brain areas and peripheral tissues were analyzed in C57BL/KsJ mice. Littermate control (+/?) and diabetic (db/db) mice were pulse-treated (60) min with 10 mu Ci of 3H-P at either 8 or 16 weeks of age. Subsequently, the peripheral tissues and brains were dissected, weighed, digested and the amount of incorporated 3H-P assessed. The pituitary, amygdala, septum and hypothalamus were found to concentrate the highest levels of 3H-P of all the brain areas examined. The brain areas of 16-week-old (+/?) mice accumulated higher concentrations of 3H-P than the comparable 8-week-old brain tissues. In addition, all the brain areas of 8-week-old (db/db) mice accumulated equal or more 3H-P than the comparable (+/?) brains. By 16 weeks of age, however, the 3H-P accumulation rate was significantly higher in all brain areas of (+/?), as compared to (db/db), mice. Of the peripheral tissues examined, the ovary, uterus, pancreas, kidney and mesometrial fat pad consistently exhibited the highest rates of 3H-P accumulation in both (+/?) and (db/db) mice. By 16 weeks of age, all peripheral tissues of (+/?) mice exhibited greater accumulation rates of 3H-P than the comparable (db/db) tissues. Following 4 days of estradiol treatment (10 micrograms/day s.c.), the 3H-P accumulation rates in 16-week-old (+/?) and (db/db) brain were essentially equal. Only the hypothalamus, septum and amygdala of the (db/db) mice failed to normalize to (+/?) levels following estradiol treatment. In a similar manner, the pancreas, uterus, ovary and fat of (db/db) mice exhibited 3H-P accumulation rates similar to those of (+/?) mice following estradiol treatment. These data indicate that estradiol therapy effectively normalizes the normal age- and diabetes-related declines in brain and peripheral tissue sensitivity and/or responsitivity to progesterone in C57BL/KsJ mice.

Age Factors↗
PubMedDate not supplied

Utilization of 14C-tyrosine in brain and peripheral tissues of developmentally protein malnourished rats.

Prior studies of developmentally protein malnourished rats have reported substantial changes in brain and peripheral utilization of 14C-leucine, 14C-phenylalanine, and 14C-tryptophan. In the present study rats born to dams fed a low protein diet (8% casein) compared to the offspring of control rats fed a normal diet (25% casein) showed few significant differences in the uptake and incorporation of 14C-tyrosine into brain and peripheral tissues from birth to age 21 days. At birth, the 8% casein pups exhibited significant decreases in brain and peripheral tissue incorporation of tracer only at short post-injection times (10 and 20 min), but not at longer intervals (90 and 180 min). During ontogenetic development (Days 5-21), the 8% casein rats showed significant increases in uptake of 14C-tyrosine into the brain and peripheral tissues on Day 11 and a significantly higher percent incorporation of tracer into brain protein on Day 21 as compared to the 25% casein rats. For the most part, there were no significant changes in incorporation of radioactivity in peripheral tissues for the 2 diet groups on these post-birth days. Overall, the data indicates that developmental protein malnutrition causes relatively fewer changes in brain and peripheral utilization of the semi-essential amino acid tyrosine than those observed in previous studies with essential amino acids.

Animals↗
PubMed1995

Distribution of thyrotropin-releasing hormone receptor mRNA in rat peripheral tissues.

Since the thyrotropin-releasing hormone receptor (TRH-R) cDNA was isolated, the distribution of TRH-R mRNA has been investigated in the central nervous system (CNS) and the pituitary. However, there has been less genetical studies on the distribution of TRH-R mRNA in the peripheral tissues, although TRH exists not only in CNS but also in the peripheral tissues. In this study we investigated the distribution of TRH-R mRNA in rat peripheral tissues by reverse transcription-polymerase chain reaction (RT-PCR) and Northern blot analysis. TRH-R mRNA was detected in almost all of the peripheral tissues tested, although the amount varied considerably depending on the tissues. In the uterus, thymus, ovary, and testis, TRH-R mRNA levels appeared to be relatively high. These results suggest that TRH and its receptor have specific functions in the peripheral tissues as well as in CNS and in the pituitary.

Alternative Splicing↗
PubMed1992

The effect of morphine tolerance dependence and abstinence on immunoreactive dynorphin (1-13) levels in discrete brain regions, spinal cord, pituitary gland and peripheral tissues of the rat.

The effect of morphine tolerance dependence and protracted abstinence on the levels of dynorphin (1-13) in discrete brain regions, spinal cord, pituitary gland and peripheral tissues was determined in male Sprague-Dawley rats. Of all the tissues examined, the highest level of dynorphin (1-13) was found to be in the pituitary gland. Among the brain regions and spinal cord examined, the levels of dynorphin (1-13) in descending order were: hypothalamus, spinal cord, midbrain, pons and medulla, hippocampus, cortex, amygdala and striatum. The descending order for the levels of dynorphin (1-13) in peripheral tissues was: adrenals, heart and kidneys. In morphine tolerant rats, the levels of dynorphin (1-13) increased in amygdala but were decreased in pons and medulla. In morphine abstinent rats, the levels of dynorphin (1-13) were increased in amygdala, hypothalamus and hippocampus. The levels of dynorphin (1-13) were increased in pituitary but decreased in spinal cord and remained so even during protracted abstinence. The levels of dynorphin (1-13) in the peripheral tissues of morphine tolerant rats were unaffected. However, in the heart and kidneys of morphine abstinent rats, the levels of dynorphin (1-13) were increased significantly. It is concluded that both morphine tolerance and abstinence modify the levels of dynorphin (1-13) in pituitary, central and peripheral tissues. Morphine abstinence differed from non-abstinence process in that there were additional changes (increases) in the levels of dynorphin (1-13) in brain regions (hypothalamus and hippocampus) and peripheral tissues (heart and kidneys) and may contribute to the symptoms of the morphine abstinence syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed2001

SCN efferents to peripheral tissues: implications for biological rhythms.

The suprachiasmatic nucleus (SCN) is the principal generator of circadian rhythms and is part of an entrainment system that synchronizes the animal with its environment. Here, we review the possible communication of timing information from the SCN to peripheral tissues involved in regulating fundamental physiological functions as revealed using a viral, transneuronal tract tracer, the pseudorabies virus (PRV). The sympathetic nervous system innervation of the pineal gland and the sympathetic outflow from brain to white adipose tissue were the first demonstrations of SCN-peripheral tissue connections. The inclusion of the SCN as part of these and other circuits was the result of lengthened postviral injection times compared with those used previously. Subsequently, the SCN has been found to be part of the sympathetic outflow from the brain to brown adipose tissue, thyroid gland, kidney, bladder, spleen, adrenal medulla, and perhaps the adrenal cortex. The SCN also is involved in the parasympathetic nervous system innervation of the thyroid, liver, pancreas, and submandibular gland. Individual SCN neurons appear connected to more than one autonomic circuit involving both sympathetic and parasympathetic innervation of a single tissue, or sympathetic innervation of two different peripheral tissues. Collectively, the results of these PRV studies require an expansion of the traditional roles of the SCN to include the autonomic innervation of peripheral tissues and perhaps the modulation of neuroendocrine systems traditionally thought to be controlled solely by hypothalamic stimulating/inhibiting factors.

Animals↗
PubMed1985

Evidence that beta-endorphin binds to specific receptors in rat peripheral tissues and stimulates the adenylate cyclase-adenosine 3',5'-monophosphate system.

With the use of [125I]acetyl human beta-endorphin (Ac-hBE), specific binding sites for beta-endorphin (BE) were identified in the liver, kidney, adrenal, spleen, and testis of adult male rats, whereas specific BE-binding sites were not present in the ventral prostate or pancreas. In those tissues containing specific BE-binding sites, microsomal membranes (15,000-100,000 X g pellet) exhibited higher BE-binding capacity than the crude homogenate (125-100,000 X g pellet). The binding of BE was saturable, and maximal, specific binding was achieved with a 60-min incubation at 22 C. Furthermore, optimal BE binding was dependent on the presence of magnesium chloride. Scatchard analysis of BE binding to hepatic membranes revealed the existence of two classes of binding sites. One class had an apparent Ka of 0.019 X 10(9) M-1 and a lower number of binding sites (9.1 pmol BE/mg protein), whereas the other class had a lower affinity (apparent Ka of 0.0006 X 10(9) M-1) and a higher number of binding sites (159 pmol/mg protein). Specific BE binding to hepatic membranes was inhibited (80-100%) by rat AcBE-(1-27) and -(1-31), nonacetylated rat BE-(1-31), and human beta-lipotropin. At substantially higher peptide concentrations (greater than 10(-5) M), gamma-endorphin, met-enkephalin, or leu-enkephalin inhibited BE binding by 20-40%. In addition, opiate receptor-binding drugs, such as morphine and naloxone, at 10(-5) M did not alter BE binding to hepatic membranes. Incubation of hepatic membranes with BE induced a dose-related increase in membrane adenylate cyclase activity, and 0.5 X 10(-10) M BE resulted in a maximal enhancement of adenylate cyclase activity to 148% above control values. Water-deprived or salt-loaded male rats with chronically lowered immunoreactive plasma BE exhibited substantially increased BE binding to adrenal and kidney tissue. Specific binding sites for BE occur in a variety of peripheral tissues, and alterations of circulating BE result in changes in the capacity of certain peripheral tissues to bind BE. Finally, occupancy of specific BE-binding sites in peripheral tissue stimulates the adenylate cyclase-cAMP system, which suggests that the peripheral actions of circulating BE may be mediated via this system.

Adenylyl Cyclases↗
PubMed2002

mRNA distribution analysis of human TRPC family in CNS and peripheral tissues.

The mammalian homologues of the Drosophila transient receptor potential (TRP) channel are plasma membrane proteins involved in the regulation of cellular Ca(2+) influx. These ion channels can be activated subsequent to either depletion of Ca(2+) from internal stores or through receptor-mediated processes. The mRNA expression patterns of several individual mammalian short transient receptor potential channels (TRPCs) have been described. Cross-comparisons between these data, however, are at best difficult predominantly due to the non-quantitative methods used. Furthermore there is limited data on the expression of TRPC family members in human tissues. In the present study we used a single technique, namely TaqMan real-time quantitative RT-PCR, to investigate the mRNA distribution of human TRPC1, TRPC3, TRPC4, TRPC5, TRPC6 and TRPC7 (hTRPCs) in discrete human brain areas, peripheral tissues as well as a panel of cell-lines. All hTRPCs studied were widely expressed within CNS and significant peripheral expression was often observed. Despite this, each channel exhibited a distinctive hallmark distribution profile. hTRPC1 was widely expressed in CNS and peripheral tissues, whereas hTRPC3 and hTRPC5 were predominantly expressed in tissues of CNS. hTRPC4 mRNA was detected in CNS and certain peripheral tissues such as bone, heart and prostate. hTRPC6 was homogeneously expressed throughout the CNS and peripheral tissues with the highest levels in placenta and lung. hTRPC7 mRNA was also broadly expressed in CNS as well as some peripheral tissues. The pattern of expression of the TRPCs was quite different in the various cell lines examined. TRPC3 and TRPC6 were selectively present in HEK-293 cells whilst TRPC1 was broadly distributed in the cell lines analyzed. In contrast TRPC4 and TRPC5 mRNAs were predominantly expressed in HK-2 and HEK-293 cell lines respectively. TRPC7 was selectively expressed in COS-1, COS-7 and HK-2 cell lines. These results show tissue- and cell-specific co-expression of multiple TRPC forms indicating widespread potential for formation of heteromeric channels. These data will be useful in the complex task of relating channel subunit composition to function in native cells.

Animals↗
PubMed1987

Peripheral tissue insulin sensitivity in healthy elderly subjects.

To determine whether the decline in glucose tolerance with age is related to changes in peripheral tissue insulin sensitivity, 11 healthy older (65-85 years) and 12 healthy younger (20-38 years) subjects, matched for physical activity and body mass index, were studied. The glucose-insulin infusion technique, in which glucose and insulin are infused at constant rates over 150 min, was used to assess peripheral tissue insulin sensitivity. The metabolic clearance rate (MCR) of glucose, which reflects peripheral tissue insulin sensitivity, is derived from the resulting steady-state blood glucose. Fasting blood glucose was similar in the two groups, but mean blood glucose 2 h after an oral glucose load was higher in the older group. MCR of glucose expressed per kilogram lean body mass was almost identical in both groups (13.3 +/- 1.3 vs. 13.5 +/- 1.3 ml/kg lean body mass/min, respectively). Evidence of decreased glucose tolerance with normal peripheral tissue insulin sensitivity suggests that changes in other factors may be more important than previously recognised.

Adult↗
PubMed1975

Distribution of 125I-labeled rat growth hormone in regional brain areas and peripheral tissue of the rat.

The uptake of intraperitoneally injected 125I-labeled rat growth hormone into brain and peripheral tissues was measured in normal and hypophysectomized adult rats. A significant level of radioactivity was observed in the seven brain regions examined -- the telencephalon, diencephalon, midbrain, pons-medulla, cerebellum, pineal and pituitary glands. The pineal and pituitary glands, which are outside the blood-brain barrier, contained three to four times the concentration of radioactivity of the other brain regions. Compared to brain, the level of radioactivity was much higher in peripheral tissues (the diaphragm, kidney, serum and liver). For example, the serum contained ten times the level of radioactivity of most brain regions. For a given tissue, however, the normal and hypophysectomized rats showed a comparable amount of 125I-growth hormone. Trichloroacetic acid precipitates from each tissue sample showed that peripheral tissues had a higher proportion of radioactivity (35-48% of total tissue radioactivity) than the brain samples (13-26%). The data support the view that growth hormone, or a metabolite can enter the central nervous system and may directly affect on-going metabolic processes.

Animals↗
PubMed1986

Octadecaneuropeptide, benzodiazepine ligand, -like immunoreactivity in rat central nervous system, plasma and peripheral tissues.

Using a specific radioimmunoassay we have investigated the distribution of octadecaneuropeptide (a putative endogenous ligand at the benzodiazepine receptor)-like immunoreactivity (ODN-IR) in rat brain and peripheral tissues. Highest concentrations in brain were found in the hypothalamus, cerebellum and substantia nigra. Significant concentrations of ODN-IR were found in all peripheral tissues studied and in plasma. Chromatographic analysis revealed several molecular forms; one major form, indistinguishable from the synthetic peptide, was found predominantly in peripheral tissues and in plasma, while another major form, of higher molecular weight, was found in brain, peripheral tissues and plasma. Although ODN-IR was present in the synaptosomal fraction, concentrations in the microsomal fraction were higher than for other neuropeptides studied.

Animals↗