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- W1965304328 abstract "Summary: Prejunctional β-adrenoceptor-mediated modulation of sympathetic neurotransmission was studied in desipramine-pretreated canine blood-perfused gracilis muscle. Overflow of endogenous noradrenaline (NA) to venous plasma and vasoconstriction reflect pre- and postjunctional events in this in vivo model. The nonselective β-adrenoceptor agonist isoprenaline (15 nM in arterial plasma) and the β2-selective agonist rimiterol (50 nM) caused similar vasodilatation (35–40% increase in vascular conductance, p < 0.01), enhancement of nerve stimulation-evoked vasoconstriction ( + 20–25%, p < 0.01), and NA overflow (+13%, p < 0.05). Isoprenaline, 3 nM, evoked vasodilatation but did not alter NA overflow. Blockade of β2-adrenoceptors by ICI 118,551 increased basal vascular tone (+ 9%, p < 0.01) and reduced nerve stimulation-evoked vasoconstriction (-7%, p &;lt; 0.05), but failed to alter NA overflow significantly (-12%, p = 0.12). ICI 118,551 blocked all responses to the β-adrenoceptor agonists. Thus, prejunctional β2-adre-noceptor-mediated facilitation of sympathetic neurotransmission could be demonstrated in vivo, but the effects were modest. Previous experiments, however, have demonstrated a considerably larger influence of α-adrenoceptor-mediated prejunctional modulation in this model. Hence, prejunctional modulation via β-adreno-ceptors appears to be of subordinate importance when compared with the α-adrenoceptor-mediated inhibitory mechanism under these physiological conditions." @default.
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- W1965304328 date "1987-10-01" @default.
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- W1965304328 title "Prejunctional β2-Adrenoceptor -Mediated Enhancement of Noradrenaline Release in Skeletal Muscle Vasculature In Situ" @default.
- W1965304328 doi "https://doi.org/10.1097/00005344-198710000-00008" @default.
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