INCREASES IN ARTERIAL BLOOD-PRESSURE IN THE RAT IN RESPONSE TO A NEW VERTEBRATE NEUROPEPTIDE, LPLRF-AMIDE, AND A RELATED MOLLUSCAN PEPTIDE, FMRFAMIDE
INCREASES IN ARTERIAL BLOOD-PRESSURE IN THE RAT IN RESPONSE TO A NEW VERTEBRATE NEUROPEPTIDE, LPLRF-AMIDE, AND A RELATED MOLLUSCAN PEPTIDE, FMRFAMIDE
复制标题
DOI：
10.1016/0167-0115(84)90062-4
复制
发表时间：
1984-01-01
影响因子：
--
通讯作者：
DOCKRAY, GJ
中科院分区：
文献类型：
--
作者：
BARNARD, CS;DOCKRAY, GJ
用鸡脑中的一种新肽LPLRFamide [leucylprolyl leucylarginyl phenylalaninamide]和免疫化学相关的软体动物[Macrocalista nimbosa]神经肽FMRFamide [phenylalanyl methionylarginyl phenylalaninamide]诱发麻醉大鼠的血管加压反应。剂量为50-200 nmol. kg-1，静脉注射，两种肽均使动脉压迅速升高，并在1-2分钟内恢复到基础水平。当以相似剂量脑池内给药时，两种肽再次升高动脉压，但达到峰值反应的时间（1-2分钟）和反应持续时间（5-8分钟）延长。脑池内注射而非静脉注射LPLRFamide后出现显著、可逆、特异性快速耐受，表明通过这些途径给药后作用部位不同。乙啶和酚妥拉明阻断了对静脉注射和脑池内给药的反应，而六甲双铵显著降低了对脑池内给药的反应。因此，通过静脉注射和脑池内途径，反应可能是由交感神经末梢释放去甲肾上腺素[去甲肾上腺素，NE]介导的。在肾上腺切除术和普萘洛尔后，对静脉内（但不是脑池内）LPLRF酰胺的反应增加，表明从肾上腺髓质释放的肾上腺素可能在β-肾上腺素水平起作用。引起血管扩张的肾上腺素受体。这些观察结果的生理学意义仍有待确定，但重要的是，与FMRFamide和LPLRFamide免疫化学相关的肽发生在与自主控制有关的大鼠大脑区域。
Vasopressor responses in urethane-anesthetized rats were evoked by a new peptide from chicken brain, LPLRFamide [leucylprolyl leucylarginyl phenylalaninamide], and the immunochemically related molluscan [Macrocallista nimbosa] neuropeptide, FMRFamide [phenylalanyl methionylarginyl phenylalaninamide]. In doses of 50-200 nmol .cntdot. kg-1, i.v., both peptides produced a rapid increase in arterial pressure that returned to basal in 1-2 min. When given intracisternally in similar doses the 2 peptides again increased arterial pressure, but the time to peak response (1-2 min) and the duration of the responses (5-8 min) were prolonged. There was a marked, reversible, specific, tachyphylaxis following intracisternal but not i.v. injection of LPLRFamide, indicating separate sites of action after administration by these routes. Guanethidine and phentolamine blocked the responses to both i.v. and intracisternal administration, and hexamethonium significantly reduced the response to intracisternal administration. Both by i.v. and intracisternal routes it is therefore likely that responses are mediated by noradrenaline [norepinephrine, NE] release from sympathetic endings. Following adrenalectomy and propranolol the response to i.v. (but not intracisternal) LPLRFamide was increased, suggesting that epinephrine released from the adrenal medulla might act at .beta.-adrenoreceptors causing vasodilatation. The physiological significance of these observations remains to be established, but it is significant that peptides immunochemically related to FMRFamide and LPLRFamide occur in areas of rat brain concerned with autonomic control.