Tanabe A, Naruse M, Naruse K, Ito F, Yoshimoto T, Seki T, Demura R, Demura H, Toma H, Inagami T
Department of Urology, Kidney Center, Tokyo Women's Medical University, Japan.
Horm Metab Res. 1999 Jul;31(7):429-34. doi: 10.1055/s-2007-978768.
The angiotensin II (Ang II) type 1 (AT1) receptor is highly expressed on juxtaglomerular (G) cells and is assumed to be involved in the negative short loop feedback regulation of renin secretion and in the suppression of Ang II-mediated JG cell proliferation and/or growth. However, as JG cell tumor is rare, expression and pathophysiological significance of AT1 receptor expression in JG cell tumor remain unknown. In the present study, we investigated renin responses to various treatments, including the angiotensin converting enzyme inhibitor captopril, and correlated the results with AT1 and Ang II type 2 (AT2) receptor mRNA expression levels in two cases of JG cell tumor. Whereas plasma renin activity (PRA) did not show any significant change in Case 1, it was increased by 72% in Case 2 in response to captopril challenge. In concordance with these results, AT1 receptor mRNA was not detected in tumor tissue of Case 1 but was clearly demonstrated in the tumor of Case 2. AT2 receptor mRNA expression was not detected in either of the cases. In contrast to captopril challenge, PRA was suppressed by 30% in Case 1 and 42% in Case 2 in response to saline infusion, and was increased by 230% in Case 1 and 59% in Case 2 in response to furosemide-upright posture for 2 h. These results suggest that the short loop feedback inhibition of renin secretion by Ang II in JG cell tumor is closely related to AT1 receptor expression levels in the tumor tissue. In addition, the result suggested that despite its autonomy, renin secretion from JG cell tumor is still under physiological regulatory control.
血管紧张素II（Ang II）1型（AT1）受体在肾小球旁（JG）细胞上高度表达，被认为参与肾素分泌的负性短环反馈调节以及抑制Ang II介导的JG细胞增殖和/或生长。然而，由于JG细胞瘤罕见，AT1受体在JG细胞瘤中的表达及其病理生理意义仍不清楚。在本研究中，我们调查了两例JG细胞瘤对包括血管紧张素转换酶抑制剂卡托普利在内的各种治疗的肾素反应，并将结果与AT1和血管紧张素II 2型（AT2）受体mRNA表达水平相关联。在病例1中，血浆肾素活性（PRA）未显示任何显著变化，而在病例2中，对卡托普利激发试验的反应使其增加了72%。与这些结果一致，在病例1的肿瘤组织中未检测到AT1受体mRNA，但在病例2的肿瘤中清晰地检测到。在两个病例中均未检测到AT2受体mRNA表达。与卡托普利激发试验相反，在病例1中，盐水输注使PRA降低了30%，在病例2中降低了42%，而在病例1中，速尿直立位2小时使PRA增加了230%，在病例2中增加了59%。这些结果表明，JG细胞瘤中Ang II对肾素分泌的短环反馈抑制与肿瘤组织中AT1受体表达水平密切相关。此外，结果表明，尽管JG细胞瘤具有自主性，但其肾素分泌仍受生理调节控制。
