Background. The kidney has a high rate of oxygen usage (Q(o2)) that is clos
ely dependent on tubular Na+ transport (T-Na) However, little is known conc
erning the regulation of the cortical partial pressure of oxygen (pO(2)).
Methods. First, the pO(2) 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 Wister Kyoto (WKY) and spontane
ously hypertensive rats (SHRs) using an ultramicrocoaxial O-2 electrode. We
next assessed the determinants of Q(o2) and tubular reabsorption of sodium
(T-Na) for whether they could account for any differences in renal cortica
l pO(2) in SHRs.
Results. The pO(2) in the EA was reduced 40 to 50% compared with arterial v
alues but was similar in the two strains (WKY rats 45 +/- 2 vs. SHRs 41 +/-
1 mm Hg, P = NS). The pO(2)-value in the PT, DT, and SC did not differ wit
hin strains. All were significantly (P < 0.001) lower in SHRs (for example,
pO(2) in PT of WKY rats 39 +/- 1 vs. SHRs, 30 +/- 1 mm Hg). The pO(2) in t
he renal vein was above that at any site in the EA or the cortex, implying
a precapillary shunting of O-2 from the artery to vein. SHRs had reduced re
nal blood flow (RBF) leading to a reduced (P < 0.05) rate of O-2 delivery (
WKY rats 42 +/- 6 vs. SHRs 30 +/- 1 mu mol . min(-1) . g(-1)) and a reduced
glomerular filtration rate, leading to a lower (P < 0.001), T-Na (WKYs 115
+/- 9 vs. SHRs 66 +/- 8 <mu>mol . min(-1) . g(-1)). However, despite the 4
3% reduction in T-Na, the renal O-2 usage was not significantly different b
etween strains (WKY rats 7.6 +/- 0.8 vs. SHRs 9.0 +/- 1.0 mu mol . min(-1)
. g(-1)). Therefore, the SHRs had a sharp reduction (P < 0.001) in the O-2
efficiency for Na+ reabsorption (T-Na/Q(o2); WKY rats 15.1 +/- 1.6 vs. SHRs
7.3 +/- 1.0 <mu>mol(-1)).
Conclusions. A precapillary O-2 Shunt reduces the pO(2) of cortical nephron
s. The pO(2) is reduced further in SHRs because of less efficient O-2 usage
for Na+ transport.