Fluid volume or arterial pressure, that is the question

Abstract

How is blood pressure controlled? Not few will say that long-term blood pressure is determined by the renal medulla (Mattson, 2003), which is also pivotal in volume homeostasis. Fluid volume and electrolyte concentration are of primary importance and it seems hardly possible for them to be entirely subordinated to the demands of arterial pressure. A clue to understanding priorities the renal medulla must make is obtained by investigating renal medullary circulation: vasa recta are very long vessels that supply this region with blood and act together with the tubular network in adjusting renal medullary tonicity. The amount of fluids being retained from the renal collecting ducts heavily depends on the osmotic gradient between the collecting duct fluid and the medulla. If this osmotic gradient is actively controlled in accordance with the demands of arterial pressure, then this can be taken as an indication of the pivotal role of the renal medulla in long-term pressure control. On the other hand if renal circulation is adjusted in order to maintain the osmotic gradient, it seems as if volume electrolyte homeostasis prevails over the requirements of arterial pressure control. In this issue of The Journal of Physiology, Dobrowolski & Sadowski (2005) provide important information with regard to the inter-relationship of renal medullary tonicity and medullary blood flow. Changes in medullary interstitial tonicity were induced by inhibiting Na+–K+–2Cl− cotransport in the ascending limb of the loop of Henle. In response to this intervention, medullary blood flow decreased in parallel to medullary ionic tonicity. A possible implication of this experiment is that the medulla itself can control its circulation in to match the demands of maintaining medullary tonicity. How does this come about? It is probably related to the renin–angiotensin system and to prostaglandins. The vasoconstrictory effect of angiotensin II (Ang II) is less pronounced in the renal medulla as compared to the renal cortex. Indeed, very recently, augmented medullary blood flow has been found in response to Ang II (Mattson & Meister, 2005). This is probably due to concurrently released vasodilators, such as NO (Cowley et al. 2003) and/or prostaglandins. Dobrowolski & Sadowski blocked prostaglandin synthesis by indomethacin. This manoeuvre not only reduced medullary blood flow but also significantly attenuated the decrease in renal medullary blood flow in response to reducing medullary tonicity. Thus, the authors conclude that the tonicity of the medulla is an important controller of medullary blood flow. A new piece in the puzzle in the role of the medulla for arterial blood pressure and volume electrolyte homeostasis seems to have been added by Dobrowolski & Sadowski (2005). The demonstration that medullary tonicity is not simply a function of medullary blood flow, but that medullary blood flow can be adjusted according to the needs of medullary tonicity, extends our understanding considerably. It is becoming clearer that the renal medulla is a key regulator in volume and electrolyte homeostasis independently of arterial blood pressure.