title: Nephron pO2 and renal oxygen usage in the hypertensive rat kidney.
abstract: BACKGROUND
  The kidney has a high rate of oxygen usage (QO2) that is closely dependent on tubular Na+ transport (TNa). However, little is known concerning the regulation of the cortical partial pressure of oxygen (pO2).
  
  
  METHODS
  First, the pO2 was measured in the outer cortical proximal (PT) and distal tubules (DT), efferent arterioles (EA), and superficial (SC) and deep cortical (DC) tissues in normotensive Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHRs) using an ultramicrocoaxial O2 electrode. We next assessed the determinants of QO2 and tubular reabsorption of sodium (TNa) for whether they could account for any differences in renal cortical pO2 in SHRs.
  
  
  RESULTS
  The pO2 in the EA was reduced 40 to 50% compared with arterial values but was similar in the two strains (WKY rats 45 +/- 2 vs. SHRs 41 +/- 1 mm Hg, P = NS). The pO2 value in the PT, DT, and SC did not differ within strains. All were significantly (P < 0. 001) lower in SHRs (for example, pO2 in PT of WKY rats 39 +/- 1 vs. SHRs, 30 +/- 1 mm Hg). The pO2 in the renal vein was above that at any site in the EA or the cortex, implying a precapillary shunting of O2 from the artery to vein. SHRs had reduced renal blood flow (RBF) leading to a reduced (P < 0.05) rate of O2 delivery (WKY rats 42 +/- 6 vs. SHRs 30 +/- 1 micromol. min-1. g-1) and a reduced glomerular filtration rate, leading to a lower (P < 0.001), TNa (WKYs 115 +/- 9 vs. SHRs 66 +/-8 micromol. min-1. g-1). However, despite the 43% reduction in TNa, the renal O2 usage was not significantly different between strains (WKY rats 7.6 +/- 0.8 vs. SHRs 9.0 +/- 1.0 micromol. min-1. g-1). Therefore, the SHRs had a sharp reduction (P < 0.001) in the O2 efficiency for Na+ reabsorption (TNa/QO2; WKY rats 15.1 +/- 1.6 vs. SHRs 7.3 +/-1.0 micromol-1).
  
  
  CONCLUSIONS
  A precapillary O2 shunt reduces the pO2 of cortical nephrons. The pO2 is reduced further in SHRs because of less efficient O2 usage for Na+ transport.
authors.affiliation: Division of Nephrology and Hypertension, Georgetown University Medical Center, Washington D.C. 20007, USA.
authors.forename: W J
authors.initials: WJ
authors.lastname: Welch
authors.forename: H
authors.initials: H
authors.lastname: Baumgärtl
authors.forename: D
authors.initials: D
authors.lastname: Lübbers
authors.forename: C S
authors.initials: CS
authors.lastname: Wilcox
mesh_terms: D000042:Absorption; D000818:Animals; D001160:Arterioles; D001682:Biological Availability; D005919:Glomerular Filtration Rate; D007668:Kidney / Q000378:metabolism*; D007672:Kidney Cortex / Q000378:metabolism; D007684:Kidney Tubules / Q000378:metabolism; D008297:Male; D009399:Nephrons / Q000378:metabolism*; D010100:Oxygen / Q000097:blood / Q000378:metabolism*; D010101:Oxygen Consumption; D010313:Partial Pressure; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012016:Reference Values; D012079:Renal Circulation; D012964:Sodium / Q000378:metabolism; D014680:Veins
chemical_list: D012964:Sodium; D010100:Oxygen