title: Impaired myogenic constriction of the renal afferent arteriole in a mouse model of reduced βENaC expression.
abstract: Previous studies demonstrate a role for β epithelial Na(+) channel (βENaC) protein as a mediator of myogenic constriction in renal interlobar arteries. However, the importance of βENaC as a mediator of myogenic constriction in renal afferent arterioles, the primary site of development of renal vascular resistance, has not been determined. We colocalized βENaC with smooth muscle α-actin in vascular smooth muscle cells in renal arterioles using immunofluorescence. To determine the importance of βENaC in myogenic constriction in renal afferent arterioles, we used a mouse model of reduced βENaC (βENaC m/m) and examined pressure-induced constrictor responses in the isolated afferent arteriole-attached glomerulus preparation. We found that, in response to a step increase in perfusion pressure from 60 to 120 mmHg, the myogenic tone increased from 4.5 ± 3.7 to 27.3 ± 5.2% in +/+ mice. In contrast, myogenic tone failed to increase with the pressure step in m/m mice (3.9 ± 0.8 to 6.9 ± 1.4%). To determine the importance of βENaC in myogenic renal blood flow (RBF) regulation, we examined the rate of change in renal vascular resistance following a step increase in perfusion pressure in volume-expanded animals. We found that, following a step increase in pressure, the rate of myogenic correction of RBF is inhibited by 75% in βENaC m/m mice. These findings demonstrate that myogenic constriction in afferent arterioles is dependent on normal expression of βENaC.
authors.affiliation: Department of Physiology and Biophysics and the Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, 2500 North State St., Jackson, MS 39216-4505, USA.
authors.forename: Ying
authors.initials: Y
authors.lastname: Ge
authors.forename: Kimberly
authors.initials: K
authors.lastname: Gannon
authors.forename: Monette
authors.initials: M
authors.lastname: Gousset
authors.forename: Ruishing
authors.initials: R
authors.lastname: Liu
authors.forename: Beau
authors.initials: B
authors.lastname: Murphey
authors.forename: Heather A
authors.initials: HA
authors.lastname: Drummond
mesh_terms: D000199:Actins / Q000378:metabolism / Q000502:physiology; D000818:Animals; D030801:Animals, Genetically Modified; D001160:Arterioles / Q000502:physiology*; D001794:Blood Pressure / Q000235:genetics / Q000502:physiology; D003627:Data Interpretation, Statistical; D053503:Epithelial Sodium Channels / Q000235:genetics / Q000502:physiology*; D007678:Kidney Glomerulus / Q000098:blood supply / Q000378:metabolism; D051379:Mice; D009129:Muscle Tonus / Q000235:genetics / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D012079:Renal Circulation / Q000235:genetics / Q000502:physiology*; D014655:Vascular Resistance / Q000235:genetics / Q000502:physiology; D014661:Vasoconstriction / Q000235:genetics / Q000502:physiology
chemical_list: D000199:Actins; D053503:Epithelial Sodium Channels; C507049:Scnn1b protein, mouse