Medullary Oxygen Tension and Perfusion of the Medulla

Oxygen tension in the medulla of the kidney is low, 10 to 25 mmHg. This is predicted to be a consequence of the countercurrent arrangement of vasa recta because oxygen in DVR blood diffuses to AVR to be shunted back to the cortex. Several hormonal systems play a role in the protection of the medulla from ischemic insult. Each shares the ability to enhance medullary blood flow and inhibit salt reabsorption by nephrons. Hypothetically this should have a dual effect to enhance the supply of oxygen and simultaneously reduce the demand for O2 consumption. One example is cyclooxygenase (COX) production of vasodilatory prostaglandins. Medullary perfusion is sensitive to COX inhibition, and renomedullary interstitial cells release prostaglandin E2 (PGE2) in response to Angll and bradykinin. Apparently, the cylooxygenase-2 isoform is responsible because Angll reduces medullary blood flow in COX2- but not COXl-deficient mice. In most vascular beds, ischemia favors generation of adenosine, a paracrine agent that enhances blood flow through local vasodilation. Within the renal medulla (but not the cortex) adenosine acts as a vasodilator and inhibits salt reabsorption by the medullary thick ascending limb of Henle (mTAL). It is reasonable to hypothesize that adenosine produced by the mTAL diffuses to and dilates DVR on the periphery of vascular bundles. Adenosine A1 and A2 receptor stimulation constricts and dilates DVR, respectively.

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