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PubMed1983

Changes of catecholamines in central and peripheral tissues and in the urines of deoxycorticosterone--salt hypertensive rats.

The catecholamine concentrations in the urines and in the tissues of the kidney, heart, striatum, and hypothalamus of control rats and rats treated with deoxycorticosterone and salt for 2-week and 5-week periods were measured and compared. In 2-week-treated rats there were no changes in blood pressure and catecholamines. In 5-week-treated rats, the blood pressure increased from 117 +/- 5 to 152 +/- 5 mmHg (1 mmHg = 0.13 kPa) and there was an increase of urinary dopamine, norepinephrine, and epinephrine. The kidney and heart tissues of the hypertensive rats showed a decrease of norepinephrine while in the hypothalamus all three catecholamines were increased. These data suggest that dopamine and epinephrine may also be involved in the sympathetic dysfunction in deoxycorticosterone--salt hypertension. They demonstrate for the first time an increase of dopamine, norepinephrine, and epinephrine in the hypothalamus of deoxycorticosterone--salt hypertensive rats.

Animals↗
PubMed1994

Kynurenic acid distribution into brain and peripheral tissues of mice.

Kynurenic acid (KYN), an antagonist of excitatory amino acid receptors, is a putative antidote against neuroexcitatory amino acid toxicity. We studied various doses (0.05-3.17 mmol/kg, i.p.) and the effects of probenecid coadministration (0.70 mmol/kg, i.p.) on tissue distribution of KYN in male and female Swiss-Webster mice. After injection of [3H]KYN, samples of brain, heart, liver, kidney, skeletal muscle, and gut were collected at selected times and assayed for KYN by liquid scintillation counting. The substance was absorbed rapidly and distributed into all tissues. Its content (nmol/g, mean +/- SE) at 60 min was 0.26 +/- 0.05, 1.80 +/- 0.05, and 40.4 +/- 8.1 in brain (for 0.05, 0.53, and 3.17 mmol/kg), 1.43 +/- 0.11, 14.3 +/- 3.7, and 212 +/- 32 in heart, 1.16 +/- 0.21, 10.6 +/- 2.6, and 254 +/- 21 in liver, and 7.41 +/- 2.65, 180 +/- 63, and 1899 +/- 254 in kidney. Net accumulation of KYN in brain was much lower than in other tissues. Probenecid increased KYN concentration in brain 2.5-fold. Peak brain:blood concentration ratio occurred between 60 and 180 min, was inversely associated with dose, and was not affected by probenecid. Although brain content was similar, female mice had an earlier peak brain:blood ratio (120 min) than males (180 min) for the 0.05 mmol/kg dose. Our results suggest the presence of a restricted transfer process for KYN with delayed egress from brain.

Animals↗
PubMed1993

Liver and peripheral tissue glycogen metabolism in obese mice: effect of a mixed meal.

Glycogen metabolism in the liver, skeletal muscle, cardiac muscle, and white adipose tissue was studied in gold thioglucose (GTG) obese mice after fasting and during refeeding. Prolonged (48 h) fasted control and GTG mice were refed with standard laboratory diet for 24 h. During fasting and refeeding, the changes in glycogen content and the activity of glycogen synthase I and R and phosphorylase alpha in the liver were similar in lean and GTG mice. However, the glycogen storage in the livers from GTG mice was always greater than that in lean animals. In GTG mice the activity of liver glycogen synthase I and R was significantly higher than that in lean animals 3 and 6 h after refeeding. The activity of liver phosphorylase alpha in GTG mice was higher than that in lean mice after refeeding. There were no significant differences in the glycogen content of white adipose tissue, cardiac muscle, and skeletal muscle from lean and GTG mice during the entire study. The results of this study suggest that increased glycogen storage in the liver is a major alteration in nonoxidative glucose metabolism and contributes to the development of insulin resistance and glucose intolerance in GTG obese mice.

Analysis of Variance↗
PubMed1994

Insulin selectively attenuates breakdown of nonmyofibrillar proteins in peripheral tissues of normal men.

The role of insulin to control protein synthesis and degradation in the human leg and forearm was investigated in eight healthy individuals. The glucose clamp technique with simultaneous infusion of crystalline amino acids were used to create hyperinsulinemia (100-120 mU/l) in combination with euglycemia and elevated plasma concentrations of amino acids (> 4 mmol/l). A primed constant infusion with L-[U-14C]tyrosine and L-[phenyl-2H5]phenylalanine was used for simultaneous measurements of the disposal (protein synthesis) and the release (protein degradation) of tyrosine and phenylalanine, respectively, across the leg and forearm before and during hyperinsulinemia. The balance of 3-methylhistidine was also determined as a measure of muscle breakdown. Insulin stimulated tissue glucose and net amino acid uptake across the arm and leg tissues, whereas the disposal of both tyrosine and phenylalanine (protein synthesis) was not stimulated across the arm and the leg during hyperinsulinemia. The release of tyrosine and phenylalanine was significantly decreased from both leg and arm tissues (protein degradation) in response to insulin. However, the release of 3-methylhistidine from skeletal muscles was totally unaffected by hyperinsulinemia. We conclude that it is unlikely that insulin contributes to the normal stimulation of protein synthesis during feeding in humans and that insulin has no effect on breakdown of the large myofibrillar protein pool in skeletal muscles in unstressed individuals.

Adult↗
PubMed1986

New proglumide-analogue CCK receptor antagonists: very potent and selective for peripheral tissues.

The present study evaluates the ability of two recently synthesized analogues of proglumide, both 4-benzamido-N,N-di-alkyl-glutaramic acid derivatives, to act as cholecystokinin receptor antagonists. Both new antagonists inhibited cholecystokinin-stimulated amylase release and, similarly, binding of 125I-cholecystokinin to isolated rat pancreatic acini. These effects displayed competitive kinetics; both antagonists showed no agonist activity and were specific in that only those secretagogues were inhibited that interact with the cholecystokinin receptor. Both antagonists also inhibited binding of 125I-cholecystokinin to mouse pancreatic membrane particles similarly to results with rat pancreatic acini. With the more potent of the two new antagonists, half-maximal inhibition of action and binding of cholecystokinin was observed with low concentrations of approximately 10(-7) M; compared with proglumide, the new antagonists were as much as 4,000 times more potent. Unlike proglumide, which inhibits binding of cholecystokinin to pancreas and brain tissue similarly, both antagonists inhibited binding of cholecystokinin to the pancreas at much lower concentrations compared with brain. The more potent of the inhibitors was 300 times more potent in inhibiting binding of cholecystokinin to pancreatic tissues compared with brain.

Amylases↗
PubMed2006

Intermittent peripheral tissue ischemia during coronary ischemia reduces myocardial infarction through a KATP-dependent mechanism: first demonstration of remote ischemic perconditioning.

Remote ischemic preconditioning reduces myocardial infarction (MI) in animal models. We tested the hypothesis that the systemic protection thus induced is effective when ischemic preconditioning is administered during ischemia (PerC) and before reperfusion and examined the role of the K(+)-dependent ATP (K(ATP)) channel. Twenty 20-kg pigs were randomized (10 in each group) to 40 min of left anterior descending coronary artery occlusion with 120 min of reperfusion. PerC consisted of four 5-min cycles of lower limb ischemia by tourniquet during left anterior descending coronary artery occlusion. Left ventricular (LV) function was assessed by a conductance catheter and extent of infarction by tetrazolium staining. The extent of MI was significantly reduced by PerC (60.4 +/- 14.3 vs. 38.3 +/- 15.4%, P = 0.004) and associated with improved functional indexes. The increase in the time constant of diastolic relaxation was significantly attenuated by PerC compared with control in ischemia and reperfusion (P = 0.01 and 0.04, respectively). At 120 min of reperfusion, preload-recruitable stroke work declined 38 +/- 6% and 3 +/- 5% in control and PerC, respectively (P = 0.001). The force-frequency relation was significantly depressed at 120 min of reperfusion in both groups, but optimal heart rate was significantly lower in the control group (P = 0.04). There were fewer malignant arrhythmias with PerC during reperfusion (P = 0.02). These protective effects of PerC were abolished by glibenclamide. Intermittent limb ischemia during myocardial ischemia reduces MI, preserves global systolic and diastolic function, and protects against arrhythmia during the reperfusion phase through a K(ATP) channel-dependent mechanism. Understanding this process may have important therapeutic implications for a range of ischemia-reperfusion syndromes.

Adenosine Triphosphate↗
PubMed1989

Tumor necrosis factor enhances glucose uptake by peripheral tissues.

Anesthetized dogs received a constant intravenous infusion of tumor necrosis factor (TNF) or saline over 6 h. Glucose kinetics were studied by determining the rate of glucose turnover and hindlimb substrate flux. Cardiovascular responses were monitored and concentrations of counterregulatory hormones were also measured. TNF infusion caused a fall in blood glucose concentration from 4.6 +/- 0.1 to 3.9 +/- 0.2 mmol/l by 6 h (P less than 0.05). This mild hypoglycemia was associated with increased circulating levels of cortisol, glucagon, and epinephrine. The rate of glucose production increased from 26.5 +/- 2.1 to 32.5 +/- 0.7 mumol.min-1.kg body wt-1 (P less than 0.05) over the 6-h infusion period; this response was associated with increased glucose disappearance (26.4 +/- 2.2 to 32.7 +/- 0.9 mumol.min-1.kg body wt-1, P less than 0.05) and enhanced clearance (5.7 +/- 0.5 to 9.0 +/- 0.6 ml.min-1.kg body wt-1, P less than 0.05). As blood glucose levels fell, hindlimb glucose uptake and glucose clearance increased markedly in TNF-infused animals as compared with controls despite a 50% fall in mean serum insulin concentration. The exchange of lactate, pyruvate, and total amino acid nitrogen across the hindlimbs was similar in both groups of animals. However, arterial concentrations of lactate and pyruvate rose to two to three times their initial values. The hypoglycemia associated with the infusion of TNF results from a disparity between the rate of glucose appearance and disappearance. There is an increased uptake of glucose across the hindlimb; this response appears to be independent of insulin concentrations and may be related to direct effects of TNF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

Role of peripheral tissue receptors in stimulation of ventilation by 2,4-dinitrophenol.

Previous workers have demonstrated that hindlimb receptors can mediate some portion of the increase in VE elicited by 2,4-dinitrophenol (DNP). Liang and Hood have recently demonstrated that these hindlimb receptors communicate with the respiratory center via afferent pathways of the lumbar spinal cord. Accordingly, to determine the quantitative contribution of these hindlimb receptors to increases in VE elicited by DNP (4 mg/kg), we compared two groups of animals with respect to ventilatory, metabolic, and thermal responses elicited by this drug. Group I animals underwent complete transection of the spinal cord at the first lumbar level, whereas the spinal cord in Group II animals remained intact. Our results indicate that Group I and Group II animals did not differ with respect to increases in VE, VO2, and rectal temperature elicited by DNP. These results suggest that hindlimb receptors do not play an obligatory role in mediating increases in VE elicited by DNP. Therefore, these observations raise the possibility that multiple afferent pathways may exist for stimulation of VE by DNP.

Animals↗
PubMed1981

Neuronal survival and peripheral tissue size during human embryogenesis: study of a partial twinning.

The relationship between somatic tissue size and development of the nervous system was studied in a partially divided human uniovular twin. In the neck region where tissues were symmetrical in each twin the spinal cords, sensory ganglia and sympathetic ganglia were also normally formed. The bodies remained fused below the necks, but the spinal cords and related neuronal structures had developed separately. Mirror image asymmetry of tissue size existed in relationship to each spinal cord. The asymmetry was reflected in size and neuron content of motor and sensory structures. Stellate ganglia on the sides of the missing arms were also hypoplastic. This abnormal human development reproduces animal experiments in which limb ablation reduces embryogenetic survival of related neurons. It is indicates that human neurons are affected by alterations in tissue bulk during ontogenesis.

Embryo, Mammalian↗
PubMed1994

Differential expression of five somatostatin receptor subtypes, SSTR1-5, in the CNS and peripheral tissue.

Somatostatin regulates endocrine and exocrine secretion, acts as a neurotransmitter/neuro-modulator and possesses antiproliferative properties. These diverse physiological effects are mediated by G-protein coupled receptors of which at least five subtypes have been cloned (SSTR1-5). Here, we have investigated the tissue distribution pattern of mRNAs encoding the five SRIF receptor subtypes in the adult rat by RT-PCR analysis and in situ hybridization histochemistry. All five receptor subtypes were found to be expressed simultaneously in brain and pituitary by RT-PCR. Besides, the in situ hybridization results clearly show a distinct but overlapping expression pattern of SSTR1-5 mRNA in the central nervous system as was found by RT-PCR for the periphery. Such distinct SRIF receptor expression may contribute to the selective biological functions of the receptor subtypes.

Animals↗
PubMed2006

Knockdown expression and hepatic deficiency reveal an atheroprotective role for SR-BI in liver and peripheral tissues.

Scavenger receptor SR-BI has been implicated in HDL-dependent atheroprotective mechanisms. We report the generation of an SR-BI conditional knockout mouse model in which SR-BI gene targeting by loxP site insertion produced a hypomorphic allele (hypomSR-BI). Attenuated SR-BI expression in hypomSR-BI mice resulted in 2-fold elevation in plasma total cholesterol (TC) levels. Cre-mediated SR-BI gene inactivation of the hypomorphic SR-BI allele in hepatocytes (hypomSR-BI-KO(liver)) was associated with high plasma TC concentrations, increased plasma free cholesterol/TC (FC/TC) ratio, and a lipoprotein-cholesterol profile typical of SR-BI-/- mice. Plasma TC levels were increased 2-fold in hypomSR-BI and control mice fed an atherogenic diet, whereas hypomSR-BI-KO(liver) and SR-BI-/- mice developed severe hypercholesterolemia due to accumulation of FC-rich, VLDL-sized particles. Atherosclerosis in hypomSR-BI mice was enhanced (2.5-fold) compared with that in controls, but to a much lower degree than in hypomSR-BI-KO(liver) (32-fold) and SR-BI-/- (48-fold) mice. The latter models did not differ in either plasma lipid levels or in the capacity of VLDL-sized lipoproteins to induce macrophage cholesterol loading. However, reduced atherosclerosis in hypomSR-BI-KO(liver) mice was associated with decreased lesional macrophage content as compared with that in SR-BI-/- mice. These data imply that, in addition to its major atheroprotective role in liver, SR-BI may exert an antiatherogenic role in extrahepatic tissues.

ATP Binding Cassette Transporter, Subfamily G, Mem↗
PubMed2007

Bimodal clock gene expression in mouse suprachiasmatic nucleus and peripheral tissues under a 7-hour light and 5-hour dark schedule.

Using the mPer1::luc real-time monitoring technique, the authors observed the bimodal patterns of mPer1 bioluminescence on each side of the SCN, in parallel with maintaining synchronization between the left and right sides of the SCN under an artificial light:dark:light:dark (LDLD) 7:5:7:5 condition. In situ hybridization analysis of mPer1 and mBmal1 mRNA distribution in the SCN showed that in 1 photophase (morning photophase; M) of LDLD, the mPer1 level in the ventrolateral-like (VL-like) subdivision of the SCN was higher than that in the dorsomedial-like (DM-like) subdivision, and this regional distribution pattern was reversed in another photophase (evening photophase; E). In contrast, the mBmal1 level was higher in the DM-like subdivision than in the VL-like subdivision in the M phase, and this distribution changed in the E phase. The prokineticin 2 (PK2) mRNA that encodes an SCN output molecule that is thought to transmit the circadian locomotor rhythms was reduced in both the DM-like and VL-like SCN and did not clearly correlate with the activity under the LDLD condition. The expression of mPer1 and mPer2 in the liver was clearly bimodal, whereas the expressions of other clock genes were not synchronized to the LDLD condition. These results may provide important insights into the mechanism underlying the splitting or bimodal rhythms that may in turn facilitate the understanding of the ability to measure the seasonal day length in mammals.

Animals↗
PubMed1987

Immunocytochemical localization of monoamine oxidases A and B in human peripheral tissues and brain.

Monoamine oxidases (MAO; EC 1.4.3.4.) A and B occur in the outer mitochondrial membrane and oxidize a number of important biogenic and xenobiotic amines. Monoclonal antibodies specific for human MAO A or B and immunocytochemical techniques were used to visualize the respective enzymes in human placenta, platelets, lymphocytes, liver, brain, and a human hepatoma cell line. MAO A was observed in the syncytiotrophoblast layer of term placenta, liver, and a subset of neurons in brain, but was not observed in platelets or lymphocytes, which are known to lack type A enzyme. MAO B was observed in platelets, lymphocytes, and liver, but not in placenta, which contains little or no MAO B. MAO B was also observed in a subset of neurons in the brain that was distinct from that which contained MAO A. MAO A and MAO B were also observed in some glia. Unlike most tissues examined, liver cells appeared to contain both forms of the enzyme. These studies show that MAO A and MAO B can be specifically visualized by immunocytochemical means in a variety of human cells and tissues and can provide a graphic demonstration of the high degree of cell specificity of expression of the two forms of the enzyme.

Antibodies, Monoclonal↗