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首页> 外文期刊>Clinical nephrology >Renal and blood pressure effects of moxonidine and clonidine in spontaneously hypertensive rats.
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Renal and blood pressure effects of moxonidine and clonidine in spontaneously hypertensive rats.

机译：莫索尼定和可乐定对自发性高血压大鼠的肾脏和血压影响。

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Recently we could demonstrate that the imidazoline receptor agonist moxonidine exerts specific renal effects in Sprague Dawley rats [Hohage et al. 1997]. Interestingly, the effects of this compound are attenuated in one kidney-one clip hypertensive rats [Li et al. 1994]. In this study, we therefore investigated the effects of moxonidine as compared to clonidine in genetically determined spontaneously hypertensive rats. Moxonidine in a concentration of 0.5 mg/kg b.w.i.v. induced a significant and long-lasting increase of both urine flow from 11.9 +/- 2.1 microliters/min x 100 g b.w. to 50.3 +/- 12.5 microliters/min x 100 g b.w. and of Na(+)-excretion from 2.2 +/- 0.5 mumol/min x 100 g b.w. to 8.4 +/- 1.9 mumol/min x 100 g b.w. In contrast to moxonidine, the effects of clonidine (0.5 mg/kg b.w.i.v.) on urine flow and Na(+)-excretion were negligible. The antagonists idazoxan, effaroxan and rauwolscine abolished the effects of moxonidine on urine flow and Na(+)-excretion, whereas 4-aminopyridine, phenformine and 1,2,3,4-tetrahydro-9-aminoacridine, which have been described to interact with imidazoline binding sites, had no effect. Addition of the antagonists idazoxan, effaroxan and rauwolscine attenuated the initial blood pressure increase immediately after intravenous application, whereas 4-aminopyridine, phenformine and 1,2,3,4-tetrahydro-9-aminoacridine had no influence on this side-effect. Our results provide further evidence that imidazoline receptor agonists such as moxonidine exhibit renal effects, different from the modulation in urine flow and Na(+)-excretion following renal alpha 2 adrenoceptor stimulation. An upregulation of imidazoline receptors in hypertension may contribute to the effects observed.
机译：最近，我们可以证明咪唑啉受体激动剂莫索尼定在Sprague Dawley大鼠中发挥特定的肾脏作用[Hohage等。 1997]。有趣的是，在一只肾一夹式高血压大鼠中，这种化合物的作用减弱了[Li et al。 1994]。因此，在这项研究中，我们在基因确定的自发性高血压大鼠中研究了可乐定与可乐定的作用。莫索尼定的浓度为0.5 mg / kg b.w.i.v.导致尿液流量显着且持久地从11.9 +/- 2.1微升/分钟x 100克体重增加。至50.3 +/- 12.5微升/分钟x 100克重量Na（+）排泄量从2.2 +/- 0.5摩尔/分钟x 100克重量至8.4 +/- 1.9摩尔/分钟x 100克重量与莫索尼定相反，可乐定（0.5 mg / kg b.w.i.v.）对尿流和Na（+）排泄的影响可忽略不计。拮抗剂依达唑沙星，依法沙星和劳伍西星消除了莫索尼定对尿流和Na（+）-排泄的影响，而4-氨基吡啶，苯甲双胍和1,2,3,4-四氢-9-氨基ac啶已被描述为相互作用与咪唑啉结合位点没有影响。静脉内应用后，拮抗剂伊达唑烷，依法洛沙星和劳伍西星的加入会减弱最初的血压升高，而4-氨基吡啶，苯甲双胍和1,2,3,4-四氢-9-氨基ac啶对此副作用没有影响。我们的结果提供了进一步的证据，表明咪唑啉受体激动剂（如莫索尼定）表现出肾脏作用，不同于肾脏α2肾上腺素能受体刺激后尿流和Na（+）排泄的调节。高血压中咪唑啉受体的上调可能有助于观察到的影响。

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