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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of insulin and norepinephrine on glucose transport, glucose uptake, and cell respiration were investigated in isolated rat brown adipocytes. Glucose transport and uptake were determined using [U-14C]-D-glucose and 2-deoxy-[1,2-3H]-D-glucose, respectively. Brown adipocyte respiration was measured polarographically. Dose-response experiments revealed that insulin stimulated D-glucose transport and 2-deoxyglucose uptake between 10(-11) and 10(-7) M with a maximal four- to sixfold stimulation. In the absence of insulin, norepinephrine concentrations ranging from 10(-7) to 10(-7) M also enhanced glucose transport and uptake with a maximal two- to fourfold stimulation. Experiments with alpha- and beta-adrenergic agonists and antagonists showed that the effect of norepinephrine was predominantly mediated via beta-adrenergic pathways. Dibutyryl cyclic AMP and 3-isobutyl-1-methylxanthine also increased glucose transport, suggesting that the effects of norepinephrine are cyclic AMP dependent. Moreover, norepinephrine (10(-8) M) enhanced insulin sensitivity for glucose transport [half-maximum velocity constant (1/2 V max)] but failed to potentiate insulin responsiveness (Vmax). On the other hand, insulin (10(-9) M) had no effect on basal respiration but rapidly inhibited the calorigenic effect of norepinephrine (10(-7) M) by greater than 50%. These results demonstrate that 1) in the absence of insulin, physiological concentrations of norepinephrine stimulate glucose transport via beta-adrenergic pathways, 2) the neurohormone synergistically potentiates brown adipocyte submaximal insulin responses for glucose transport, and 3) insulin counteracts the effects of norepinephrine on brown adipocyte thermogenesis despite the fact that both hormones enhance glucose uptake.
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PMID:Stimulation of glucose transport by insulin and norepinephrine in isolated rat brown adipocytes. 247 26

The effect of adrenaline (Ad) on muscarinic transmission was examined in B neurones of bullfrog sympathetic ganglia by using intracellular and voltage-clamp recording methods. Bath-application of Ad (5-500 microM) caused a depression of the slow excitatory postsynaptic potential (EPSP) elicited by repetitive stimulations of preganglionic nerve fibres in the presence of curare (30 microM). Ad also depressed the 'muscarinic' ACh potential induced by ionophoretic application of ACh directly to curarized sympathetic neurones in a concentration-dependent manner. Isoprenaline mimicked the effect of Ad in producing the inhibition of the 'muscarinic' ACh potential. Propranolol antagonized the inhibitory action of Ad. Dibutyryl adenosine 3',5'-monophosphate had no significant effect on the 'muscarinic' ACh potential. Under voltage-clamp conditions, Ad caused an inward current associated with inhibition of the M-current (Brown and Adams 1980). Ad depressed the amplitude of slow postsynaptic currents produced by applications of ACh and muscarinic. At a concentration of 100 microM, Ad produced a 68 +/- 8% (n = 12) depression of the amplitude of the muscarinic ACh current. The inhibition of muscarinic transmission induced by Ad is due to a direct suppression of the muscarinic current at the postsynaptic membrane in bullfrog sympathetic ganglia.
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PMID:Adrenaline inhibits muscarinic transmission in bullfrog sympathetic ganglia. 254 82