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在自发性高血压大鼠高血压发展过程中神经肽Y对血管功能的调节作用

Modulation of vascular function by neuropeptide Y during development of hypertension in spontaneously hypertensive rats.

作者信息

Zukowska-Grojec Z, Golczynska M, Shen G H, Torres-Duarte A, Haass M, Wahlestedt C, Myers A K

机构信息

Department of Physiology and Biophysics, Georgetown University Medical Center, Washington, D.C. 20007.

出版信息

Pediatr Nephrol. 1993 Dec;7(6):845-52. doi: 10.1007/BF01213372.

DOI:10.1007/BF01213372
PMID:7907499
Abstract

Neuropeptide Y (NPY) is a sympathetic cotransmitter and a platelet-derived factor which causes vasoconstriction, potentiation of norepinephrine (NE) action, and vascular mitogenic effects. Reciprocally, NE markedly enhances the actions of NPY. We studied vasopressor effects of NPY and sources of peptide release during the development of hypertension in spontaneously hypertensive rats (SHR). Conscious SHR (4 and 16 weeks old) had higher resting plasma levels of NE and epinephrine than age-matched Wistar-Kyoto (WKY) rats, but similar NPY immunoreactivity (NPY-ir) levels in platelet-poor plasmas (PPP). In both strains, NPY-ir levels in PPP were higher in 4-week-old than in older rats. However, at all ages (4-24 weeks) SHR had markedly elevated NPY-ir content in platelet-rich-plasmas than WKY rats, although levels declined with age and hypertension. In the superior mesenteric artery, NPY-ir content (per mg) was significantly higher in 4-week-old but lower in 16-week-old SHR than in WKY rats, suggesting greater sympatho-neural NPY stores and release (leading to depletion) during the development of hypertension. Four-week-old SHR also tended to have higher NPY-ir content in the adrenal medullae and coeliac ganglia but a lower content in the kidney than WKY rats; these differences disappeared with age. Pressor responsiveness to alpha-agonists and NPY were similar in both strains at 4 weeks. While unchanged by age in WKY rats, adrenergic and NPY-mediated vasopressor responses became augmented in 16- to 24-week-old SHR (compared with WKY rats); this hyperresponsiveness was not completely abolished by ganglionic blockade and not observed with vasopressin.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

神经肽Y(NPY)是一种交感神经共递质和血小板衍生因子,可引起血管收缩、增强去甲肾上腺素(NE)的作用以及产生血管有丝分裂效应。相反,NE可显著增强NPY的作用。我们研究了自发性高血压大鼠(SHR)高血压发展过程中NPY的升压作用及肽释放的来源。清醒的SHR(4周龄和16周龄)静息血浆中NE和肾上腺素水平高于年龄匹配的Wistar-Kyoto(WKY)大鼠,但血小板贫浆(PPP)中的NPY免疫反应性(NPY-ir)水平相似。在两种品系中,4周龄大鼠PPP中的NPY-ir水平均高于老年大鼠。然而,在所有年龄段(4 - 24周),SHR富含血小板血浆中的NPY-ir含量均显著高于WKY大鼠,尽管其水平随年龄和高血压的发展而下降。在肠系膜上动脉中,4周龄SHR的NPY-ir含量(每毫克)显著高于WKY大鼠,但16周龄时则低于WKY大鼠,这表明在高血压发展过程中交感神经NPY储存和释放更多(导致耗竭)。4周龄的SHR肾上腺髓质和腹腔神经节中的NPY-ir含量也往往高于WKY大鼠,但肾脏中的含量低于WKY大鼠;这些差异随年龄增长而消失。4周龄时,两种品系对α-激动剂和NPY的升压反应相似。WKY大鼠的肾上腺素能和NPY介导的升压反应不随年龄变化,而16至24周龄的SHR(与WKY大鼠相比)则增强;这种高反应性不能被神经节阻断完全消除,且血管加压素未观察到这种情况。(摘要截断于250字)

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本文引用的文献

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神经刺激诱导自发性高血压大鼠中神经肽Y的释放及血管紧张素II的调节作用
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