Evidence that renal arterial-venous oxygen shunting contributes to dynamic regulation of renal oxygenation

Abstract

Renal blood flow (RBF) can be reduced in rats and rabbits by up to 40% without significant changes in renal tissue Po(2). We determined whether this occurs because renal oxygen consumption changes with RBF or due to some other mechanism. The relationships between RBF and renal cortical and medullary tissue P(O(2)) and renal oxygen metabolism were determined in the denervated kidneys of anesthetized rabbits under hypoxic, normoxic, and hyperoxic conditions. During artificial ventilation with 21% oxygen (normoxia), RBF increased 32 +/- 8% during renal arterial infusion of acetylcholine and reduced 31 +/- 5% during ANG II infusion. Neither infusion significantly altered arterial pressure, tissue P(O(2)) in the renal cortex or medulla, nor renal oxygen consumption. However, fractional oxygen extraction fell as RBF increased and the ratio of oxygen consumption to sodium reabsorption increased during ANG II infusion. Ventilation with 10% oxygen (hypoxia) significantly reduced both cortical and medullary P(O(2)) (60-70%), whereas ventilation with 50% and 100% oxygen (hyperoxia) increased cortical and medullary P(O(2)) (by 62-298 and 30-56%, respectively). However, responses to altered RBF under hypoxic and hyperoxic conditions were similar to those under normoxic conditions. Thus renal tissue P(O(2)) was relatively independent of RBF within a physiological range (+/-30%). This was not due to RBF-dependent changes in renal oxygen consumption. The observation that fractional extraction of oxygen fell with increased RBF, yet renal parenchymal P(O(2)) remained unchanged, supports the hypothesis that preglomerular diffusional shunting of oxygen from arteries to veins increases with increasing RBF, and so contributes to dynamic regulation of intrarenal oxygenation.

Regional decreases in renal oxygenation during graded acute renal arterial stenosis: a case for renal ischemia

“…Moreover, the reduced O 2 efficiency for sodium reabsorption may reflect the increased impact of medullary O 2 consumption occurring due to a shifting of reabsorption from paracellular to transcellular pathways, resulting in increased stoichiometric energy requirements. Furthermore, arteriovenous shunting (12,18,25) may also occur during progressive renal arterial stenosis and warrants further investigation.…”

“…Because of the parallel arrangement of descending and ascending vasa recta, important for the concentrating mechanism, the kidney is subjected to "shifting" or shunting of arterial O 2 to the venous side (11,16,25). Shunting accounts for both the higher O 2 concentration in the renal vein with respect to the superficial cortex and for the very low O 2 concentration in the renal papilla (3,25).…”

“…While the present study demonstrates variations in intrarenal P t O 2 associated with healthy kidneys in an acute situation, future studies will need to explore changes in tissue PO 2 within chronic disease. The Clark type O 2 electrodes measure O 2 through the consumption of O 2 at the tip of the electrode (11,19,20,25) and are limited by the need for penetration of the kidney capsule; however, they are considered to be a reference standard for assessment of tissue oxygenation (10). Recent advances in polymer biomaterials may offer a promising coating that may improve future sensor biocompatibility.…”

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

“…Under normal, steady-state conditions, the oxygen (O 2 ) supply to the renal tissues is well in excess of oxygen demand. Under pathological conditions, however, the delicate balance of oxygen supply compared with demand is easily disturbed owing to the unique arrangement of the renal microvasculature and its increasing numbers of diffusive shunting pathways (9,10). The renal microvasculature is serially organized, with almost all descending vasa recta emerging from the efferent arterioles of the juxtamedullary glomeruli.…”

Hypoxia Selectively Activates the CREB Family of Transcription Factors in the In Vivo Lung

“…For example, hypoxic pulmonary vasoconstriction and pulmonary hypertension develop when alveolar PO 2 is 40-60 mm Hg (2,5,13), a value that is substantially higher than that in other organs under conditions of normal oxygenation (14)(15)(16). This implies that there are specific mechanisms within the lung that are responsible for sensing and responding to changes in PO 2 , which are different from those found in other organs and tissues.…”