Decreased angiotensin II response but unaltered cardiovascular pressor response to infused norepinephrine after sodium restriction and converting enzyme inhibition.

Decreased angiotensin II response but unaltered cardiovascular pressor response to infused norepinephrine after sodium restriction and converting enzyme inhibition.
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限制钠摄入和抑制转化酶后,血管紧张素 II 反应降低,但对输注去甲肾上腺素的心血管升压反应未改变。

DOI:
10.1038/clpt.1993.50
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发表时间:
1993
影响因子:
6.7
通讯作者:
Brown,MR
Brown,MR
中科院分区:
医学2区
文献类型:
--
作者:
Mills,PJ;Dimsdale,JE;Ziegler,MG;Nelesen,RA;Brown,MR

文献摘要

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尽管研究表明卡托普利等转化酶抑制剂会影响 α-肾上腺素能生理学,但有关 α-肾上腺素能生理学的数据并不一致。因此,本研究检查了 17 名高血压受试者和 27 名血压正常受试者在限钠期间卡托普利(50 mg/天,持续 5 天)对输注去甲肾上腺素(0.01 至 0.1 μg/kg/min)的升压反应以及血管紧张素 II 和神经肽 Y 水平的影响。在安慰剂给药期间,血管紧张素 II 因注射去甲肾上腺素而显着增加(p < 0.001),但在卡托普利给药期间则没有显着增加(p = 0.15)。卡托普利导致神经肽 Y 水平下降(p= 0.02)。尽管有这些变化,卡托普利对输注去甲肾上腺素的升压反应没有变化。这些数据支持这样的结论:卡托普利的抗高血压作用与去甲肾上腺素介导的α-肾上腺素能升压调节的改变无关。神经肽Y水平降低的发现可能与卡托普利的治疗效果有关。临床药理学和治疗学(1993)53,450–456; doi:10.1038/clpt.1993.50
Although studies indicate that converting enzyme inhibitors such as captopril influence α‐adrenergic physiology, the data on α‐adrenergic physiology is inconsistent. This study therefore examined the effects of captopril (50 mg/day for 5 days) during sodium restriction on the pressor response and on angiotensin II and neuropeptide Y levels to infused norepinephrine (0.01 to 0.1 μg/kg/min) in 17 hypertensive and 27 normotensive subjects. Angiotensin II increased significantly in response to infused norepinephrine during placebo administration(p< 0.001) but not during captopril administration(p= 0.15). Neuropeptide Y levels decreased in response to captopril(p= 0.02). Despite these changes the pressor response to infused norepinephrine was unchanged with captopril. These data support the conclusion that the antihypertensive action of captopril is unrelated to alterations in norepinephrine‐mediated α‐adrenergic pressor regulation. The finding of a decrease in neuropeptide Y levels may have relevance to the therapeutic effects of captopril.Clinical Pharmacology and Therapeutics(1993)53,450–456; doi:10.1038/clpt.1993.50