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A novel role for GABA and glutamate in pericyte-mediated regulation of medullary blood flow

Dunn, Kadeshia, Kelley, Stephen P., Crawford, Carol, Wildman, Scott S.P., Peppiatt-Wildman, Claire M. (2013) A novel role for GABA and glutamate in pericyte-mediated regulation of medullary blood flow. In: The FASEB Journal. The FASEB Journal. . Federation of American Society of Experimental Biology (doi:10.1096/fj.1530-6860) (KAR id:53248)

Abstract

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 ?M) 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.

Item Type: Conference or workshop item (Poster)
DOI/Identification number: 10.1096/fj.1530-6860
Subjects: Q Science > QP Physiology (Living systems)
R Medicine
R Medicine > RM Therapeutics. Pharmacology
Divisions: Divisions > Division of Natural Sciences > Medway School of Pharmacy
Depositing User: Stephen Kelley
Date Deposited: 13 Dec 2015 13:47 UTC
Last Modified: 16 Feb 2021 13:31 UTC
Resource URI: https://kar.kent.ac.uk/id/eprint/53248 (The current URI for this page, for reference purposes)

University of Kent Author Information

Kelley, Stephen P..

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Wildman, Scott S.P..

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Peppiatt-Wildman, Claire M..

Creator's ORCID: https://orcid.org/0000-0002-4406-8571
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