title: Descending Vasa Recta Endothelial Membrane Potential Response Requires Pericyte Communication.
abstract: Using dual-cell electrophysiological recording, we examined the routes for equilibration of membrane potential between the pericytes and endothelia that comprise the descending vasa recta (DVR) wall. We measured equilibration between pericytes in intact vessels, between pericytes and endothelium in intact vessels and between pericytes physically separated from the endothelium. Dual pericyte recording on the abluminal surface of DVR showed that both resting potential and subsequent time-dependent voltage fluctuations after vasoconstrictor stimulation remained closely equilibrated, regardless of the agonist employed (angiotensin II, vasopressin or endothelin 1). When pericytes where removed from the vessel wall but retained physical contact with one another, membrane potential responses were also highly coordinated. In contrast, responses of pericytes varied independently when they were isolated from both the endothelium and from contact with one another. When pericytes and endothelium were in contact, their resting potentials were similar and their temporal responses to stimulation were highly coordinated. After completely isolating pericytes from the endothelium, their mean resting potentials became discordant. Finally, complete endothelial isolation eliminated all membrane potential responses to angiotensin II. We conclude that cell-to-cell transmission through the endothelium is not needed for pericytes to equilibrate their membrane potentials. AngII dependent responses of DVR endothelia may originate from gap junction coupling to pericytes rather than via receptor dependent signaling in the endothelium, per se.
authors.affiliation: Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland 21201, United States of America.
authors.forename: Zhong
authors.initials: Z
authors.lastname: Zhang
authors.affiliation: Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland 21201, United States of America.
authors.forename: Kristie
authors.initials: K
authors.lastname: Payne
authors.affiliation: Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland 21201, United States of America.
authors.forename: Thomas L
authors.initials: TL
authors.lastname: Pallone
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D002450:Cell Communication / Q000187:drug effects; D002469:Cell Separation; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology*; D017629:Gap Junctions / Q000187:drug effects / Q000378:metabolism; D016014:Linear Models; D008564:Membrane Potentials / Q000187:drug effects*; D018408:Patch-Clamp Techniques; D020286:Pericytes / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D014661:Vasoconstriction / Q000187:drug effects
chemical_list: D000804:Angiotensin II