Angiotensin II type 1 receptor expression in two cases of juxtaglomerular cell tumor: correlation to negative feedback of renin secretion by angiotensin II.
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.[1]References
- Angiotensin II type 1 receptor expression in two cases of juxtaglomerular cell tumor: correlation to negative feedback of renin secretion by angiotensin II. Tanabe, A., Naruse, M., Naruse, K., Ito, F., Yoshimoto, T., Seki, T., Demura, R., Demura, H., Toma, H., Inagami, T. Horm. Metab. Res. (1999) [Pubmed]
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