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In vivo imaging of the kidney in early diabetes
Author(s) -
Toma Ildiko,
Sipos Arnold,
McCulloch Fiona,
PetiPeterdi Janos
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1170-a
Subject(s) - renin–angiotensin system , endocrinology , medicine , nephron , kidney , chemistry , renal function , hemodynamics , angiotensin ii , in vivo , angiotensin ii receptor type 1 , diabetes mellitus , juxtaglomerular apparatus , macula densa , blood pressure , biology , microbiology and biotechnology
Activation of the renin‐angiotensin system (RAS) and changes in renal hemodynamics is a hallmark of the diabetic (DM) kidney. As the initial step of RAS activation, renin is synthesized and released from both the juxtaglomerular apparatus (JGA) and distal nephron (cortical collecting duct, CCD). We aimed to directly visualize heterogeneity and regulation of renin content and associated functional parameters in the DM kidney in vivo. The STZ diabetic model was applied using male, 200g Munich‐Wistar rats. Multi‐photon microscopy was used to visualize individual renin granules and to quantify basic renal functions. Both 4‐days short‐term (S) and 4‐weeks long‐term (L) DM groups developed systemic hypertension (S: 174±6, L: 143±2 mmHg), significant increases in glomerular diameter, red blood cell velocity, and single nephron glomerular filtration rate (SNGFR, S: 26±2, L: 28±3 nl/min). Both JGA and CCD renin content increased approx. 2‐fold in both S and L. Interestingly, angiotensin II (ANG II) AT1‐receptor blockade (ARB) caused a further increase in JGA renin (3‐fold vs. control), but reduced CCD renin to control levels. ARB treatment normalized blood pressure (S: 108±2, L: 91±2 mmHg) and renal hemodynamics (SNGFR S: 8±1, L: 16±2 nl/min). Munich‐Wistar DM rats develop ANG II‐dependent hypertension, and opposite to the JGA, ANG II up‐regulates renin in the CCD.