title: Mechanisms of K(+) induced renal vasodilation in normo- and hypertensive rats in vivo.
abstract: OBJECTIVE
  We investigated the mechanisms behind K(+) -induced renal vasodilation in vivo in normotensive Sprague-Dawley (SD) rats and spontaneously hypertensive rats (SHR).
  
  
  METHODS
  Renal blood flow (RBF) was measured utilizing an ultrasonic Doppler flow probe. Renal vascular resistance (RVR) was calculated as the ratio of mean arterial pressure (MAP) and RBF (RVR = MAP/RBF). Test drugs were introduced directly into the renal artery. Inward rectifier K(+) (K(ir) ) channels and Na(+) ,K(+) -ATPase were blocked by Ba(2+) and ouabain (estimated plasma concentrations ∼20 and ∼7 μm) respectively.
  
  
  RESULTS
  Confocal immunofluorescence microscopy demonstrated K(ir) 2.1 channels in pre-glomerular vessels of SD and SHR. Ba(2+) caused a transient (6-13%) increase in baseline RVR in both SD and SHR. Ouabain had a similar effect. Elevated renal plasma [K(+) ] (∼12 mm) caused a small and sustained decrease (5-13%) in RVR in both strains. This decrease was significantly larger in SHR than in SD. The K(+) -induced vasodilation was attenuated by Ba(2+) in control SD and SHR and by ouabain in SD. Nitric oxide (NO) blockade using l-NAME treatment increased MAP and decreased RBF in both rat strains, but did not affect the K(+) -induced renal vasodilation.
  
  
  CONCLUSIONS
  K(+) -induced renal vasodilation is larger in SHR, mediated by K(ir) channels in SD and SHR, and in addition, by Na(+) ,K(+) -ATPase in SD. In addition, NO is not essential for K(+) -induced renal vasodilation.
authors.affiliation: Division of Renal and Vascular Physiology, Department of Biomedical Sciences, The Panum Institute, University of Copenhagen, Denmark.  
authors.forename: L
authors.initials: L
authors.lastname: Magnusson
authors.forename: C M
authors.initials: CM
authors.lastname: Sorensen
authors.forename: T H
authors.initials: TH
authors.lastname: Braunstein
authors.forename: N-H
authors.initials: NH
authors.lastname: Holstein-Rathlou
authors.forename: M
authors.initials: M
authors.lastname: Salomonsson
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D017609:Barium Compounds / Q000494:pharmacology; D002712:Chlorides / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005455:Fluorescent Antibody Technique; D007668:Kidney / Q000098:blood supply* / Q000502:physiology; D008297:Male; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000097:blood*; D024661:Potassium Channels, Inwardly Rectifying / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051381:Rats; D011918:Rats, Inbred SHR; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation / Q000502:physiology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000187:drug effects / Q000378:metabolism; D014655:Vascular Resistance / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*
chemical_list: D017609:Barium Compounds; D002712:Chlorides; D004791:Enzyme Inhibitors; D024661:Potassium Channels, Inwardly Rectifying; C024986:barium chloride; D010042:Ouabain; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium