1. The microcirculation of the kidney is arranged in a manner that facilitates separation of blood flow to the cortex, outer medulla and inner medulla. 2. Resistance vessels in the renal vascular circuit include arcuate and interlobular arteries, glomerular afferent and efferent arterioles and descending vasa recta. 3. Vasoactive hormones that regulate smooth muscle cells of the renal circulation can originate outside the kidney (e.g. vasopressin), can be generated from nearby regions within the kidney (e.g. kinins, endothelins, adenosine) or they can be synthesized by adjacent endothelial cells (e.g. nitric oxide, prostacyclin, endothelins). 4. Vasoactive hormones released into the renal inner medullary microcirculation may be trapped by countercurrent exchange to act upon descending vasa recta within outer medullary vascular bundles. 5. Countercurrent blood flow within the renal medulla creates a hypoxic environment. Relative control of inner versus outer medullary blood flow may play a role to abrogate the hypoxia that arises from O2 consumption by the thick ascending limb of Henle. 6. Cortical blood flow is autoregulated. In contrast, the extent of autoregulation of medullary blood flow appears to be influenced by the volume status of the animal. Lack of medullary autoregulation during volume expansion may be part of fundamental processes that regulate salt and water excretion.

Pallone, Thomas L., Malcolm R. Turner, Auré lie Edwards, and Rex L. Jamison. Countercurrent exchange in the renal medulla. Am J Physiol Regul Integr Comp Physiol 284: R1153-R1175, 2003 10.1152/ ajpregu.00657.2002The microcirculation of the renal medulla traps NaCl and urea deposited to the interstitium by the loops of Henle and collecting ducts. Theories have predicted that countercurrent exchanger efficiency is favored by high permeability to solute. In contrast to the conceptualization of vasa recta as simple "U-tube" diffusive exchangers, many findings have revealed surprising complexity. Tubular-vascular relationships in the outer and inner medulla differ markedly. The wall structure and transport properties of descending vasa recta (DVR) and ascending vasa recta (AVR) are very different. The recent discoveries of aquaporin-1 (AQP1) water channels and the facilitated urea carrier UTB in DVR endothelia show that transcellular as well as paracellular pathways are involved in equilibration of DVR plasma with the interstitium. Efflux of water across AQP1 excludes NaCl and urea, leading to the conclusion that both water abstraction and diffusion contribute to transmural equilibration. Recent theory predicts that loss of water from DVR to the interstitium favors optimization of urinary concentration by shunting water to AVR, secondarily lowering blood flow to the inner medulla. Finally, DVR are vasoactive, arteriolar microvessels that are anatomically positioned to regulate total and regional blood flow to the outer and inner medulla. In this review, we provide historical perspective, describe the current state of knowledge, and suggest areas that are in need of further exploration. vasa recta; microperfusion; microcirculation; water channel; urinary concentration; permeability SINCE THE EXPERIMENTAL FINDINGS of Wirz et al. (147) led to the countercurrent theory of the urinary concentrating mechanism, as described by Hargitay and Kuhn (31), most subsequent research has focused on the countercurrent multiplier function of the loops of Henle. According to the theory, a small difference in osmotic pressure (the single effect) is multiplied by countercurrent flow in adjacent channels of the limbs of Henle's loop to produce a large axial difference in osmotic pressure between the renal cortex and the tip of the renal papilla; that is, the multiplier generates a hypertonic renal medulla. Less attention has been paid to countercurrent exchange, which is thought to preserve medullary hypertonicity rather than create it. It is generally accepted that the microcirculation of the renal medulla functions as a countercurrent exchanger that traps NaCl and urea deposited to the interstitium by the loops of Henle and collecting ducts, respectively. Early hypothetical descriptions of this process envisioned a system in which descending vasa recta (DVR) and ascending vasa recta (AVR) are parallel tubes that equilibrate by diffusion. According to that notion, blood flowing from the corticomedullary junction toward the papillary t...

We investigated the dependence of ANG II (10(-8) M)-induced constriction of outer medullary descending vasa recta (OMDVR) on membrane potential (Psim) and chloride ion. ANG II depolarized OMDVR, as measured by fully loading them with the voltage-sensitive dye bis[1,3-dibutylbarbituric acid-(5)] trimethineoxonol [DiBAC(4)(3)] or selectively loading their pericytes. ANG II was also observed to depolarize pericytes from a resting value of -55.6 +/- 2.6 to -26.2 +/- 5.4 mV when measured with gramicidin D-perforated patches. When measured with DiBAC(4)(3) in unstimulated vessels, neither changing extracellular Cl(-) concentration ([Cl(-)]) nor exposure to the chloride channel blocker indanyloxyacetic acid 94 (IAA-94; 30 microM) affected Psim. In contrast, IAA-94 repolarized OMDVR pretreated with ANG II. Neither IAA-94 (30 microM) nor niflumic acid (30 microM, 1 mM) affected the vasoactivity of unstimulated OMDVR, whereas both dilated ANG II-preconstricted vessels. Reduction of extracellular [Cl(-)] from 150 to 30 meq/l enhanced ANG II-induced constriction. Finally, we identified a Cl(-) channel in OMDVR pericytes that is activated by ANG II or by excision into extracellular buffer. We conclude that constriction of OMDVR by ANG II involves pericyte depolarization due, in part, to increased activity of chloride channels.

Water permeates many microvessel walls via a pathway shared with small hydrophilic solutes and also via an exclusive water pathway. In outer medullary descending vasa recta (OMDVR), the relationship between diffusional permeabilities to water and sodium indicates the existence of an exclusive water pathway and suggests that of a shared pathway. We investigated the latter possibility by estimating hydraulic permeability (Lp) and diffusional permeability to [3H]raffinose (P(raf)) in isolated, perfused OMDVR. The product of hydraulic permeability and osmotic reflexion coefficient of albumin (Lp sigma a) was 1.56 +/- 0.19 x 10(-6) cm.s-1.mmHg-1 (n = 28), calculated from transmural volume fluxes induced by perfusate-to-bath differences in albumin oncotic pressure (delta IIa). P(raf) in the same vessels was 40.1 +/- 7.5 x 10(-5) cm/s when delta IIa was zero. In separate experiments, sigma a was at least 0.89 +/- 0.10 (n = 17). Lp sigma a correlates with P(raf), indicating that OMDVR contain a shared pathway for convection driven by delta IIa and for diffusion of small hydrophilic solutes.