Linton-Dahlöf P
Department of Clinical Pharmacology, Gothenburg University, Sweden.
Acta Physiol Scand Suppl. 1989;586:1-85.
I. Based on experiments on the rat portal vein, it is suggested that NPY is capable of inhibiting TNS-induced release of 3H-NA from the sympathetic nerves via a prejunctional site of action, and that NPY enhances the spontaneous contractility and the vasoconstrictor response to TNS via a postjunctionally mediated mechanism. II. Based on experiments in the pithed rat, it is suggested that NPY inhibits the PNS-induced enhancement of plasma NA and A levels, and that this reflects an inhibitory effect of NPY on the release of NA from sympathetic nerve terminals and the secretion of A from the adrenal medulla. III. Based on experiments in the pithed rat, it is suggested that infusion of NPY, at subthreshold doses, potentiates the blood-pressure response to PNS and to injection of the alpha-agonist phenylephrine and that NPY in higher doses induces pressor responses, which are resistant to alpha- and beta-adrenoceptor blockade but sensitive to the calcium antagonist nifedipine. IV. Based on experiments in the pithed rat, it is suggested that A is secreted from the adrenal medulla directly into the circulating blood, since the peak plasma A level occurred immediately (0-20 s) after the initiation of PNS, and that NA and NPY are released from sympathetic nerve terminals from where the transmitters have to diffuse into the systemic circulation, since the maximal levels of circulating NA and NPY-LI were reached later (20-40 s) than A. V. Based on experiments in the pithed guinea-pig, it is suggested that the PNS-induced increase of the plasma NPY-LI level is modulated by a prejunctional alpha 2-adrenoceptor mediated inhibitory control mechanism, since the alpha 2-agonist clonidine was found to reduce and the alpha 2-antagonist yohimbine to markedly enhance the PNS-induced increase in plasma NPY-LI, whereas the alpha 1-antagonist prazosin had no effect. Furthermore, guanethidine reduced this parameter, lending further support to the assumption that circulating NPY is of sympathetic neuronal origin. VI. Based on experiments in the pithed guinea-pig, it is suggested that prejunctional facilitatory beta-adrenoceptors may also be involved in the regulation of the NPY release, since infusion of isoprenaline elicited a facilitation of the PNS-induced increase of plasma NPY-LI levels which could be antagonised by propranolol.(ABSTRACT TRUNCATED AT 400 WORDS)
一、基于对大鼠门静脉的实验，提示神经肽Y（NPY）能够通过作用于神经节前位点抑制神经降压素（TNS）诱导的交感神经释放3H-去甲肾上腺素（3H-NA），且NPY通过节后介导机制增强自发性收缩力以及对TNS的血管收缩反应。二、基于对脊髓毁损大鼠的实验，提示NPY抑制副交感神经系统（PNS）诱导的血浆去甲肾上腺素（NA）和肾上腺素（A）水平升高，这反映了NPY对交感神经末梢释放NA以及肾上腺髓质分泌A的抑制作用。三、基于对脊髓毁损大鼠的实验，提示以阈下剂量输注NPY可增强对PNS以及注射α-激动剂去氧肾上腺素的血压反应，且高剂量NPY可诱导升压反应，该反应对α和β肾上腺素能受体阻断有抗性，但对钙拮抗剂硝苯地平敏感。四、基于对脊髓毁损大鼠的实验，提示A从肾上腺髓质直接分泌入循环血液，因为血浆A水平峰值在PNS开始后立即（0 - 20秒）出现，而NA和NPY从交感神经末梢释放，递质必须从那里扩散到体循环中，因为循环中NA和NPY免疫反应性（NPY-LI）的最大水平比A出现得晚（20 - 40秒）。五、基于对脊髓毁损豚鼠的实验，提示PNS诱导的血浆NPY-LI水平升高受神经节前α2-肾上腺素能受体介导的抑制性控制机制调节，因为发现α2-激动剂可乐定可降低而α2-拮抗剂育亨宾可显著增强PNS诱导的血浆NPY-LI升高，而α1-拮抗剂哌唑嗪无作用。此外，胍乙啶降低了该参数，进一步支持循环中的NPY源自交感神经元的假设。六、基于对脊髓毁损豚鼠的实验，提示神经节前易化性β-肾上腺素能受体也可能参与NPY释放的调节，因为输注异丙肾上腺素可促进PNS诱导的血浆NPY-LI水平升高，这可被普萘洛尔拮抗。（摘要截选至400字）
