RENIN AND ANGIOTENSINOGEN GENE-EXPRESSION AND INTRARENAL RENIN DISTRIBUTION DURING ACE INHIBITION
RENIN AND ANGIOTENSINOGEN GENE-EXPRESSION AND INTRARENAL RENIN DISTRIBUTION DURING ACE INHIBITION
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DOI：
10.1152/ajprenal.1988.254.6.f900
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发表时间：
1988-06-01
影响因子：
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通讯作者：
CAREY, RM
中科院分区：
文献类型：
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作者：
GOMEZ, RA;LYNCH, KR;CAREY, RM
为了确定血管紧张素转换酶（ACE）抑制是否影响肾内肾素和血管紧张素原的合成和分布，我们将成年雄性Wistar-Kyoto大鼠（n=7）与用依那普利治疗5 d的大鼠（n=8）进行比较。利用大鼠肾素和血管紧张素原全长cdna，采用Northern和dot blot方法检测肾素和血管紧张素原mRNA水平。依那普利治疗组肾素mRNA水平是对照组的4.6倍（P < 0.05）。血管紧张素原mRNA水平无显著差异。免疫细胞化学法测定肾素在两组大鼠肾内的分布有显著差异。在对照组中，肾素定位于肾小球旁位置，而在依那普利治疗的大鼠肾脏中，传入小动脉的肾素免疫反应性远远超出了小叶间动脉方向的肾小球旁位置。在依那普利组，肾素免疫染色的传入小动脉长度百分比更高(53。17%)，高于对照组(33% +-。15)组。同样，依那普利组免疫染色的肾小球旁器械（JGA）与JGA总数之比和免疫染色的动脉与动脉总数之比更高（0.84 .+-）。0.017;0.68。+ -。0.03)高于对照组(0.67 .+-。0.034;0.43。+ -。0.045)组（P < 0.05）。我们得出结论，慢性ACE抑制增强肾内肾素合成，并增加肾素在肾小球上游和血管新部位的表达。这表明ACE抑制诱导了在基础状态下不表达肾素基因的细胞的募集。
To define whether intrarenal renin and angiotensinogen synthesis and distribution are affected by angiotensin-converting enzyme (ACE) inhibition, a control group of adult, male Wistar-Kyoto rats (n=7) was compared with a group of rats treated with enalapril (n=8) for 5 days. Kidney renin and angiotensinogen mRNA levels were detected by Northern and dot blot analysis, using full-length rat renin and angiotensinogen cDNAs. Renin mRNA levels in the enalapril-treated group were 4.6-fold higher than in the control group (P < 0.05). Angiotensinogen mRNA levels were not significantly different. The intrarenal distribution of renin assessed by immunocytochemistry was markedly different between the two groups of rats. Whereas in the control kidney renin was localized in a juxtaglomerular position, in the kidneys from enalapril-treated rats, renin immunoreactivity of the afferent arteriole extended well beyond the juxtaglomerular loci in the direction of the interlobular artery. The percent of afferent arteriolar length immunostained for renin was higher in the enalapril-treated (53 .+-. 17%) than in the control (33 .+-. 15) group. Similarly, the ratio of immunostained juxtaglomerular apparatuses (JGA) over total number of JGA and the ratio of immunostained arteries over total number of arteries were higher in the enalapril-treated (0.84 .+-. 0.017; 0.68 .+-. 0.03) than in the control (0.67 .+-. 0.034; 0.43 .+-. 0.045) group (P < 0.05). We conclude that chronic ACE inhibition enhances intrarenal renin synthesis and increases renin expression upstream from the glomerular and in new sites in blood vessels. It is suggested that ACE inhibition induces a recruitment of cells that in the basal state were not expressing the renin gene.