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A novel role for GABA and glutamate in pericyte‐mediated regulation of medullary blood flow
Author(s) -
Dunn Kadeshia Natasha,
Kelley Stephen P,
Crawford Carol,
Wildman Scott S P,
PeppiattWildman Claire M
Publication year - 2013
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.27.1_supplement.1110.13
Subject(s) - pericyte , vasa recta , glutamate receptor , kidney , chemistry , glutamate decarboxylase , vasodilation , endocrinology , medicine , endogeny , microbiology and biotechnology , biology , biochemistry , enzyme , endothelial stem cell , receptor , in vitro
GABA and its synthesising enzyme, glutamate decarboxylase, have been detected in the rat kidney [1–2]. GABA has also been found in human plasma and urine [3–4] and most recently, a renoprotective role for GABA has been suggested [5]. We are systematically investigating functional roles for GABA and glutamate in the mammalian kidney. Contractile pericytes regulate vasa recta diameter in response to a number of endogenous vasoactive agents and in doing so regulate medullary blood flow (MBF) [6]. We have utilised the live kidney slice model [6] to demonstrate GABA‐mediated constriction of vasa recta that was significantly greater at pericyte sites than at non‐pericyte sites (p< 0.01). Conversely, the GABA substrate glutamate (100 μM) caused a significantly greater vasodilation of vasa recta at pericyte sites compared to non‐pericyte sites (p< 0.05). Data presented here identifies a novel role for GABA and glutamate in pericyte‐mediated regulation of vasa recta diameter and thus MBF.