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Enhanced intrarenal receptor-mediated prorenin activation in chronic progressive anti-thymocyte serum nephritis rats on high salt intake.
Am J Physiol Renal Physiol. 2012 Jul 01; 303(1):F130-8.AJ

Abstract

Despite suppression of the circulating renin-angiotensin system (RAS), high salt intake (HSI) aggravates kidney injury in chronic kidney disease. To elucidate the effect of HSI on intrarenal RAS, we investigated the levels of intrarenal prorenin, renin, (pro)renin receptor (PRR), receptor-mediated prorenin activation, and ANG II in chronic anti-thymocyte serum (ATS) nephritic rats on HSI. Kidney fibrosis grew more severe in the nephritic rats on HSI than normal salt intake. Despite suppression of plasma renin and ANG II, marked increases in tubular prorenin and renin proteins without concomitant rises in renin mRNA, non-proteolytically activated prorenin, and ANG II were noted in the nephritic rats on HSI. Redistribution of PRR from the cytoplasm to the apical membrane, along with elevated non-proteolytically activated prorenin and ANG II, was observed in the collecting ducts and connecting tubules in the nephritic rats on HSI. Olmesartan decreased cortical prorenin, non-proteolytically activated prorenin and ANG II, and apical membranous PRR in the collecting ducts and connecting tubules, and attenuated the renal lesions. Cell surface trafficking of PRR was enhanced by ANG II and was suppressed by olmesartan in Madin-Darby canine kidney cells. These data suggest the involvement of the ANG II-dependent increase in apical membrane PRR in the augmentation of intrarenal binding of prorenin and renin, followed by nonproteolytic activation of prorenin, enhancement of renin catalytic activity, ANG II generation, and progression of kidney fibrosis in the nephritic rat kidneys on HSI. The origin of the increased tubular prorenin and renin remains to be clarified. Further studies measuring the urinary prorenin and renin are needed.

Authors+Show Affiliations

First Department of Medicine, Hamamatsu University School of Medicine, Japan. huangyanjie69@hotmail.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22496409

Citation

Huang, Yanjie, et al. "Enhanced Intrarenal Receptor-mediated Prorenin Activation in Chronic Progressive Anti-thymocyte Serum Nephritis Rats On High Salt Intake." American Journal of Physiology. Renal Physiology, vol. 303, no. 1, 2012, pp. F130-8.
Huang Y, Yamamoto T, Misaki T, et al. Enhanced intrarenal receptor-mediated prorenin activation in chronic progressive anti-thymocyte serum nephritis rats on high salt intake. Am J Physiol Renal Physiol. 2012;303(1):F130-8.
Huang, Y., Yamamoto, T., Misaki, T., Suzuki, H., Togawa, A., Ohashi, N., Fukasawa, H., Fujigaki, Y., Ichihara, A., Nishiyama, A., Senbonmatsu, T., Ikegaya, N., & Hishida, A. (2012). Enhanced intrarenal receptor-mediated prorenin activation in chronic progressive anti-thymocyte serum nephritis rats on high salt intake. American Journal of Physiology. Renal Physiology, 303(1), F130-8. https://doi.org/10.1152/ajprenal.00275.2011
Huang Y, et al. Enhanced Intrarenal Receptor-mediated Prorenin Activation in Chronic Progressive Anti-thymocyte Serum Nephritis Rats On High Salt Intake. Am J Physiol Renal Physiol. 2012 Jul 1;303(1):F130-8. PubMed PMID: 22496409.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Enhanced intrarenal receptor-mediated prorenin activation in chronic progressive anti-thymocyte serum nephritis rats on high salt intake. AU - Huang,Yanjie, AU - Yamamoto,Tatsuo, AU - Misaki,Taro, AU - Suzuki,Hiroyuki, AU - Togawa,Akashi, AU - Ohashi,Naro, AU - Fukasawa,Hirotaka, AU - Fujigaki,Yoshihide, AU - Ichihara,Atsuhiro, AU - Nishiyama,Akira, AU - Senbonmatsu,Takaaki, AU - Ikegaya,Naoki, AU - Hishida,Akira, Y1 - 2012/04/11/ PY - 2012/4/13/entrez PY - 2012/4/13/pubmed PY - 2012/9/21/medline SP - F130 EP - 8 JF - American journal of physiology. Renal physiology JO - Am. J. Physiol. Renal Physiol. VL - 303 IS - 1 N2 - Despite suppression of the circulating renin-angiotensin system (RAS), high salt intake (HSI) aggravates kidney injury in chronic kidney disease. To elucidate the effect of HSI on intrarenal RAS, we investigated the levels of intrarenal prorenin, renin, (pro)renin receptor (PRR), receptor-mediated prorenin activation, and ANG II in chronic anti-thymocyte serum (ATS) nephritic rats on HSI. Kidney fibrosis grew more severe in the nephritic rats on HSI than normal salt intake. Despite suppression of plasma renin and ANG II, marked increases in tubular prorenin and renin proteins without concomitant rises in renin mRNA, non-proteolytically activated prorenin, and ANG II were noted in the nephritic rats on HSI. Redistribution of PRR from the cytoplasm to the apical membrane, along with elevated non-proteolytically activated prorenin and ANG II, was observed in the collecting ducts and connecting tubules in the nephritic rats on HSI. Olmesartan decreased cortical prorenin, non-proteolytically activated prorenin and ANG II, and apical membranous PRR in the collecting ducts and connecting tubules, and attenuated the renal lesions. Cell surface trafficking of PRR was enhanced by ANG II and was suppressed by olmesartan in Madin-Darby canine kidney cells. These data suggest the involvement of the ANG II-dependent increase in apical membrane PRR in the augmentation of intrarenal binding of prorenin and renin, followed by nonproteolytic activation of prorenin, enhancement of renin catalytic activity, ANG II generation, and progression of kidney fibrosis in the nephritic rat kidneys on HSI. The origin of the increased tubular prorenin and renin remains to be clarified. Further studies measuring the urinary prorenin and renin are needed. SN - 1522-1466 UR - https://www.unboundmedicine.com/medline/citation/22496409/Enhanced_intrarenal_receptor_mediated_prorenin_activation_in_chronic_progressive_anti_thymocyte_serum_nephritis_rats_on_high_salt_intake_ L2 - http://www.physiology.org/doi/full/10.1152/ajprenal.00275.2011?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -