在单肾单夹高血压大鼠中，莫索尼定和利美尼定对肾脏的反应减弱。

Attenuated renal response to moxonidine and rilmenidine in one kidney-one clip hypertensive rats.

作者信息

Li P, Penner S B, Smyth D D

机构信息

Department of Pharmacology, University of Manitoba, Winnipeg, Canada.

出版信息

Br J Pharmacol. 1994 May;112(1):200-6. doi: 10.1111/j.1476-5381.1994.tb13052.x.

DOI:10.1111/j.1476-5381.1994.tb13052.x

PMID:8032642

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1910300/

Abstract

I1 non-adrenoceptor, imidazoline receptor agonists, such as moxonidine, increase urine flow rate and sodium excretion following infusion into the renal artery. The functions of these agonists in genetic and acquired models of hypertension have not been determined. 2. We therefore studied the renal effects of two known non-adrenoceptor, imidazoline receptor agonists, rilmenidine and moxonidine, in 1K-1C hypertensive and 1K-sham normotensive rats. Rilmenidine (0, 3, 10, 30 nmol kg-1 min-1) or moxonidine (0, 1, 3, 10 nmol kg-1 min-1) was infused directly into the renal artery (30 gauge needle) of 1K-sham normotensive and 1K-1C hypertensive rats. 3. In 1K-sham normotensive rats, rilmenidine and moxonidine produced dose related increases in urine flow rate, sodium excretion and osmolar clearance. Both rilmenidine and moxonidine failed to increase urine flow rate, sodium excretion and osmolar clearance in 1K-1C hypertensive rats to the same extent as in 1K-sham animals. At comparable doses, rilmenidine had no effect, while moxonidine (3 and 10 nmol kg-1 min-1) did result in a small increase in urine volume and osmolar clearance which was less than that observed in the 1K sham control animals. 4. These studies indicate that the renal effects of non-adrenoceptor, imidazoline receptor stimulation are diminished in 1K-1C hypertensive rats compared with 1K-sham normotensive rats. Whether this decrease in activity of the natriuretic non-adrenoceptor, imidazoline receptors contributes to the increase in blood pressure in the 1K-1C acquired model of hypertension remains to be determined.

摘要

I1非肾上腺素能受体、咪唑啉受体激动剂，如莫索尼定，在注入肾动脉后可增加尿流率和钠排泄。这些激动剂在高血压遗传和获得性模型中的作用尚未确定。2. 因此，我们研究了两种已知的非肾上腺素能受体、咪唑啉受体激动剂，利美尼定和莫索尼定，对1K-1C高血压大鼠和1K-假手术正常血压大鼠的肾脏影响。将利美尼定（0、3、10、30 nmol kg-1 min-1）或莫索尼定（0、1、3、10 nmol kg-1 min-1）直接注入1K-假手术正常血压大鼠和1K-1C高血压大鼠的肾动脉（30号针头）。3. 在1K-假手术正常血压大鼠中，利美尼定和莫索尼定可使尿流率、钠排泄和渗透清除率呈剂量依赖性增加。利美尼定和莫索尼定均未能使1K-1C高血压大鼠的尿流率、钠排泄和渗透清除率增加到与1K-假手术动物相同的程度。在可比剂量下，利美尼定无作用，而莫索尼定（3和l0 nmol kg-1 min-1）确实导致尿量和渗透清除率略有增加，但低于1K假手术对照动物中观察到的增加。4. 这些研究表明，与1K-假手术正常血压大鼠相比，1K-1C高血压大鼠中非肾上腺素能受体、咪唑啉受体刺激的肾脏效应减弱。这种利钠非肾上腺素能受体、咪唑啉受体活性的降低是否导致1K-1C获得性高血压模型中的血压升高仍有待确定。