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首页> 外文期刊>Hypertension: An Official Journal of the American Heart Association >Pre- and postjunctional inhibition of vascular sympathetic function by captopril in SHR. Implication of vascular angiotensin II in hypertension and antihypertensive actions of captopril.
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Pre- and postjunctional inhibition of vascular sympathetic function by captopril in SHR. Implication of vascular angiotensin II in hypertension and antihypertensive actions of captopril.

机译：卡托普利对SHR的结交前后血管交感功能的抑制作用。血管紧张素II在高血压和卡托普利的降压作用中的意义。

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The present study was designed to examine the effects of treatment of SHR with captopril, teprotide, and saralasin on vascular and cardiac responses to sympathetic nerve stimulation and angiotensin I and II (AI, AII) and norepinephrine (NE). A single dose of captopril (10 mg/kg i.v. as well as 10 and 100 mg/kg p.o.) caused significant and marked inhibition of pressor responses to sympathetic nerve stimulation in pithed SHR but cardiac responses were unaffected. Pressor responses to AI were abolished but those to AII and NE were not significantly altered. Neither teprotide nor saralasin caused consistent inhibition of sympathetic responses despite total blockade of AI and AII response respectively. Selective inhibition of pressor but not cardiac responses to sympathetic nerve stimulation was obtained after 2 weeks, 3 and 6 months of daily oral doses of captopril. In addition, postjunctional pressor responses to AI, AII, and NE were also significantly inhibited by chronic captopril treatment. Infusion of AII, bilateral nephrectomy, or pretreatment with indomethacin alone in pithed SHR receiving captopril had no effect on the inhibition of pressor responses to sympathetic stimulation. However, the combination of pretreatment of indomethacin and infusion of AII completely restored sympathetic function in SHR receiving captopril. These studies suggest that captopril has a selective inhibitory effect on vascular responses to sympathetic nerve stimulation but not on cardiac responses. Moreover, this effect may have a prejunctional component since, after acute treatment, there is no inhibitory effect on responses to AII or NE. Since, under appropriate conditions, the inhibition can be reversed by AII infusion but not nephrectomy, it is suggested that this inhibition occurs at the vascular level by inhibition of local AII formation by captopril, a site not accessible to teprotide or saralasin.
机译：本研究旨在检查卡托普利，四丙肽和aralasin对SHR的治疗对交感神经刺激和血管紧张素I和II（AI，AII）和去甲肾上腺素（NE）的血管和心脏反应的影响。单剂量卡托普利（静脉内10 mg / kg以及p.o 10和100 mg / kg）可以明显抑制SHR引起的对交感神经刺激的升压反应，但心脏反应不受影响。取消了对AI的升压反应，但对AII和NE的升压反应没有明显改变。尽管分别阻断了AI和AII应答，但是teprotide和saralasin均未引起对交感反应的持续抑制。每天口服卡托普利2周，3和6个月后，选择性抑制了对交感神经刺激的升压，但没有心脏反应。此外，慢性卡托普利治疗也显着抑制了对AI，AII和NE的结后加压反应。在接受卡托普利的髓性SHR中输注AII，双侧肾切除术或单独使用消炎痛预处理对抑制对交感刺激的升压反应没有影响。然而，消炎痛的预处理和AII输注的结合完全恢复了接受卡托普利的SHR的交感功能。这些研究表明卡托普利对交感神经刺激的血管反应具有选择性抑制作用，但对心脏反应则没有。此外，该作用可能具有连接前作用，因为在急性治疗后，对AII或NE的反应没有抑制作用。由于在适当条件下，可以通过AII输注而不能通过肾切除术来逆转这种抑制作用，因此表明这种抑制作用是通过卡托普利（对四肽或萨拉辛不易接近的部位）抑制局部AII形成而在血管水平发生的。

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