Dahlöf P, Tarizzo V I, Lundberg J M, Dahlöf C
Department of Clinical Pharmacology, Gothenburg University, Sweden.
J Auton Nerv Syst. 1991 Sep;35(3):199-210. doi: 10.1016/0165-1838(91)90098-n.
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.
在麻醉的豚鼠中，研究了一种β-肾上腺素能激动剂和一种拮抗剂对节前神经刺激（PNS）诱发的血浆神经肽Y样免疫反应性（NPY-LI）增加的影响，实验分别在存在和不存在α2-肾上腺素能拮抗剂育亨宾的情况下进行。施加四个PNS周期（8Hz，持续30秒，间隔20分钟），并分析平均动脉血压（ΔBP）、心率（ΔHR）和血浆NPY-LI（ΔNPY-LI）的增加情况。静脉输注非选择性β-激动剂异丙肾上腺素（0.15μg·kg-1·min-1）倾向于降低PNS引起的ΔBP，并在基线时显著增加心率，但不改变最大心率反应。育亨宾（1mg·kg-1静脉注射）预处理可使PNS引起的ΔBP显著增加约20%，而基础心率未观察到任何变化。非选择性β-肾上腺素能拮抗剂普萘洛尔（5mg·kg-1静脉注射）在存在和不存在育亨宾的情况下均显著降低ΔBP和ΔHR。与相应对照相比，异丙肾上腺素输注使血浆ΔNPY-LI增加37%。异丙肾上腺素的这种作用起效似乎较慢，并且可被普萘洛尔阻断，而普萘洛尔本身并未显著改变血浆ΔNPY-LI。育亨宾预处理导致血浆ΔNPY-LI增加三到四倍，在同时存在异丙肾上腺素（-39%）和普萘洛尔（-27%）的情况下略有降低。总之，交感神经传递，就神经元NPY而言，似乎有两种肾上腺素能控制机制：一种是抑制性的，一种是促进性的，分别由突触前α2-和β-肾上腺素能受体介导。如果α2-肾上腺素能受体已经使神经元NPY的释放大大增强，则无法证明促进性控制机制。
