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抑制兔脑中肾上腺素生成酶可预防单肾单夹高血压和醋酸脱氧皮质酮盐高血压。

Inhibition of adrenaline-forming enzyme in the brain prevents one-kidney, one-clip hypertension and deoxycorticosterone acetate-salt hypertension in the rabbit.

作者信息

Rosendorff C, Melamed J R, Hurwitz M L, Coull A, Jarvis A

出版信息

Clin Sci (Lond). 1982 Dec;63(6):573-6. doi: 10.1042/cs0630573.

Abstract
  1. Phenylethanolamine N-methyltransferase (PNMT) converts noradrenaline into adrenaline and brain PNMT is elevated in spontaneously hypertensive and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. In view of the evidence for the involvement of central adrenergic neurons in renal hypertension, we measured the blood pressure response in one-clip, one-kidney Goldblatt hypertensive and DOCA-salt hypertensive rabbits to the PNMT inhibitor SK&F 64139, injected into the lateral cerebral ventricles. 2. Intracerebroventricular injection of SK&F 64139 (10 micrograms/kg) significantly attenuated the mean arterial blood pressure rise in one-clip, one-kidney and DOCA-salt rabbits, at 4 and 8 weeks. 3. These findings support the idea the hypertension in this animal model required an intact adrenaline biosynthetic process, and that central catecholaminergic neurons may be involved in the pathogenesis of low-renin dependent forms of hypertension.
摘要
  1. 苯乙醇胺N-甲基转移酶(PNMT)将去甲肾上腺素转化为肾上腺素,自发性高血压大鼠和醋酸脱氧皮质酮(DOCA)-盐性高血压大鼠脑内的PNMT水平升高。鉴于有证据表明中枢肾上腺素能神经元参与肾性高血压的发生,我们测定了单夹单肾型Goldblatt高血压兔和DOCA-盐性高血压兔经侧脑室注射PNMT抑制剂SK&F 64139后的血压反应。2. 脑室内注射SK&F 64139(10微克/千克)可在4周和8周时显著减弱单夹单肾型和DOCA-盐性兔的平均动脉血压升高。3. 这些发现支持这样的观点,即该动物模型中的高血压需要完整的肾上腺素生物合成过程,并且中枢儿茶酚胺能神经元可能参与低肾素依赖性高血压形式的发病机制。

相似文献

2
Cardiovascular activity of SK&F 64139 in the hypertensive rat.SK&F 64139对高血压大鼠的心血管活性
J Cardiovasc Pharmacol. 1983 Sep-Oct;5(5):889-97. doi: 10.1097/00005344-198309000-00029.

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