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Angiotensin II (ANG II), renal perfusion pressure (RPP) and synchronization of cortical blood flow studied using laser speckle perfusion imaging (LSPI)
Author(s) -
Mitrou Nicholas,
Scully Chris,
Dymond Melissa,
Zheng Fei,
Waring Jennifer,
Braam Branko,
Chon Ki,
Cupples William
Publication year - 2012
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.26.1_supplement.690.4
Subject(s) - synchronization (alternating current) , autoregulation , perfusion , kidney , medicine , renal cortex , cortex (anatomy) , renal blood flow , chemistry , neuroscience , blood pressure , biology , mathematics , topology (electrical circuits) , combinatorics
Renal autoregulatory mechanisms, myogenic (MR) and tubuloglomerular feedback (TGF), are synchronized among neighboring nephrons. Using LSP I (Moor FLPI) we examined on a physiologically relevant scale the contribution of this synchronization, or coupling, to regulation and autoregulation of renal blood flow. In particular we explore the roles of RPP and ANG II on synchronization at the surface of the kidney cortex. A circular spatial filter (r=562±87 μm) was applied to each frame. Time‐frequency spectra were computed for each pixel and synchronization was assessed by frequency locking within MR and TGF bands. Five male Long Evans rats were studied during spontaneous pressure (SPN, 110±13 mmHg), reduced RPP (LP, 61±2), captopril (1 mg/kg, CAP, 89±12), and LP+CAP, 61±2 mmHg. Surface flux was 1679+227, 1386+172, 2076+126 and 1807+156 units, respectively. Synchronization occurred in both MR and TGF frequency bands at SPN. As expected power in these bands was markedly reduced at LP as was synchronization. Instead, a single dominant frequency developed and was widely synchronized. LP+CAP also showed reduced MR and TGF power, but neither a single dominant frequency nor wide synchronization. The data show that reduced RPP during ACE inhibition reduces synchronization of MR and TGF and suggest that ANG II is a major regulator of the radius of synchronization. Funded by CIHR MOP‐102694