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  • Title: Alpha- and beta-adrenoceptor-mediated effects on nerve stimulation-evoked release of neuropeptide Y (NPY)-like immunoreactivity in the pithed guinea pig.
    Author: Dahlöf P, Tarizzo VI, Lundberg JM, Dahlöf C.
    Journal: J Auton Nerv Syst; 1991 Sep; 35(3):199-210. PubMed ID: 1744378.
    Abstract:
    The effect of one beta-adrenoceptor agonist and one antagonist on preganglionic nerve stimulation (PNS)-evoked increase of plasma neuropeptide Y-like immunoreactivity (NPY-LI) was studied in the pithed guinea pig, both in the presence and in the absence of the alpha 2-adrenoceptor antagonist yohimbine. Four periods of PNS (8 Hz for 30 s with 20 min intervals) were applied and the increases of mean arterial blood pressure (delta BP), heart rate (delta HR) and plasma NPY-LI (delta NPY-LI) were analysed. Infusion of the non-selective beta-agonist isoprenaline (0.15 micrograms x kg-1 x min-1 i.v.) tended to reduce delta BP in response to PNS and significantly increased HR at baseline without changing the maximal HR response. Pretreatment with yohimbine (1 mg x kg-1 i.v.) significantly increased delta BP in response to PNS by about 20% without any change in basal HR being observed. The non-selective beta-adrenoceptor antagonist propranolol (5 mg x kg-1 i.v.) significantly reduced delta BP and delta HR both in the presence and in the absence of yohimbine. Isoprenaline infusion enhanced plasma delta NPY-LI by 37% in comparison with the corresponding control. This effect of isoprenaline appeared to be slow in onset and could be blocked by propranolol, which per se did not significantly change plasma delta NPY-LI. Pretreatment with yohimbine caused a three to four-fold increase in plasma delta NPY-LI, which was slightly reduced both in the presence of isoprenaline (-39%) and propranolol (-27%). In conclusion, the sympathetic neurotransmission, also with regard to neuronal NPY, seems to have two adrenergic control mechanisms: one inhibitory and one facilitatory mediated by presynaptic alpha 2- and beta-adrenoceptors, respectively. The facilitatory control mechanism could not be demonstrated if the release of neuronal NPY was already greatly enhanced by alpha 2-adrenoceptors.
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