Syncytial communication in descending vasa recta includes myoendothelial coupling.
Using dual cell patch-clamp recording, we examined pericyte, endothelial, and myoendothelial cell-to-cell communication in descending vasa recta. Graded current injections into pericytes or endothelia yielded input resistances of 220 ± 21 and 128 ± 20 MΩ, respectively (P < 0.05). Injection of positive or negative current into an endothelial cell depolarized and hyperpolarized adjacent endothelial cells, respectively. Similarly, current injection into a pericyte depolarized and hyperpolarized adjacent pericytes. During myoendothelial studies, current injection into a pericyte or an endothelial cell yielded small, variable, but significant change of membrane potential in heterologous cells. Membrane potentials of paired pericytes or paired endothelia were highly correlated and identical. Paired measurements of resting potentials in heterologous cells were also correlated, but with slight hyperpolarization of the endothelium relative to the pericyte, -55.2 ± 1.8 vs. -52.9 ± 2.2 mV (P < 0.05). During dual recordings, angiotensin II or bradykinin stimulated temporally identical variations of pericyte and endothelial membrane potential. Similarly, voltage clamp depolarization of pericytes or endothelial cells induced parallel changes of membrane potential in the heterologous cell type. We conclude that the descending vasa recta endothelial syncytium is of lower resistance than the pericyte syncytium and that high-resistance myoendothelial coupling also exists. The myoendothelial communication between pericytes and endothelium maintains near identity of membrane potentials at rest and during agonist stimulation. Finally, endothelia membrane potential lies slightly below pericyte membrane potential, suggesting a tonic role for the former to hyperpolarize the latter and provide a brake on vasoconstriction.
Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland.
Zhong
Z
Zhang
Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland.
Kristie
K
Payne
Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland tpallone@medicine.umaryland.edu.
Thomas L
TL
Pallone
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001920:Bradykinin / Q000494:pharmacology; D002450:Cell Communication / Q000187:drug effects / Q000502:physiology*; D042783:Endothelial Cells / Q000187:drug effects* / Q000502:physiology; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D007679:Kidney Medulla / Q000187:drug effects; D008564:Membrane Potentials / Q000187:drug effects* / Q000502:physiology; D018408:Patch-Clamp Techniques; D020286:Pericytes; D051381:Rats; D017207:Rats, Sprague-Dawley
D000804:Angiotensin II; D001920:Bradykinin
electrophysiology; kidney; medulla; microcirculation; pericyte; rat