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神经元降钙素基因相关肽表达的调节。血压升高的作用。

Regulation of neuronal calcitonin gene-related peptide expression. Role of increased blood pressure.

作者信息

Supowit S C, Zhao H, Wang D H, DiPette D J

机构信息

Department of Internal Medicine (Division of General Internal Medicine and Hypertension Section), University of Texas Medical Branch, Galveston 77555-1065, USA.

出版信息

Hypertension. 1995 Dec;26(6 Pt 2):1177-80. doi: 10.1161/01.hyp.26.6.1177.

DOI:10.1161/01.hyp.26.6.1177
PMID:7498991
Abstract

Calcitonin gene-related peptide (CGRP) is a potent vasodilator neuropeptide. We have previously demonstrated that CGRP mRNA levels are increased in dorsal root ganglia, and immunoreactive CGRP content is elevated in the spinal cord in mineralocorticoid-salt hypertension. Dorsal root ganglia neuronal cell bodies synthesize CGRP and send axons peripherally to blood vessels and centrally to spinal cord sites involved in blood pressure regulation. This increased synthesis of a potent vasodilator is a compensatory response to attenuate the increase in blood pressure; however, it is not known if neuronal CGRP is regulated simply by the elevated blood pressure or by changes in other parameters. To determine if elevation of blood pressure in normal rats induced by the administration of a potent vasoconstrictor can increase neuronal CGRP mRNA, 7-week-old male Sprague-Dawley rats were treated for 2 weeks with either angiotensin II (n = 6) or vehicle (n = 6) by using implanted osmotic minipumps. After the treatment period, the angiotensin II-treated rats displayed a marked increase in systolic blood pressure (angiotensin II, 217 +/- 18 versus control, 131 +/- 3 mm Hg, P < .001), and decrease in plasma renin activity (angiotensin II, 3.7 +/- 3.5 versus control, 35.9 +/- 14.2 ng.mL-1.h-1, P < .05). However, dorsal root ganglia CGRP mRNA content did not significantly differ between the two groups of rats. These results demonstrate that a marked increase in blood pressure, by itself, does not increase neuronal CGRP mRNA accumulation.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

降钙素基因相关肽(CGRP)是一种强效血管舒张神经肽。我们之前已经证明,在盐皮质激素性高血压中,背根神经节中CGRP mRNA水平升高,脊髓中免疫反应性CGRP含量增加。背根神经节神经元细胞体合成CGRP,并将轴突外周发送至血管,中枢发送至参与血压调节的脊髓部位。这种强效血管舒张剂合成的增加是对血压升高的一种代偿反应;然而,尚不清楚神经元CGRP是否仅由血压升高或其他参数的变化调节。为了确定给予强效血管收缩剂诱导的正常大鼠血压升高是否能增加神经元CGRP mRNA,使用植入式渗透微型泵对7周龄雄性Sprague-Dawley大鼠进行为期2周的治疗,一组给予血管紧张素II(n = 6),另一组给予赋形剂(n = 6)。治疗期结束后,血管紧张素II治疗的大鼠收缩压显著升高(血管紧张素II组为217±18 mmHg,对照组为131±3 mmHg,P <.001),血浆肾素活性降低(血管紧张素II组为3.7±3.5 ng·mL-1·h-1,对照组为35.9±14.2 ng·mL-1·h-1,P <.05)。然而,两组大鼠背根神经节CGRP mRNA含量无显著差异。这些结果表明,血压的显著升高本身并不会增加神经元CGRP mRNA的积累。(摘要截断于250字)

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