The relationship between kidney function, its diseases and blood pressure was a subject of number of extensive studies. The aim of this article was the attempt at completing the knowledge about renal interstitium. Renal interstitium is a three-dimensional complex structure divided into cortical and medullar part. It serves as an environment for intrarenal blood vessels and tubules and therefore it is known as a key coordinating element.
The elevated interstitium volume in the medullar part has an impast on many kidney functions, like natriuresis and is responsible for blood pressure regulation. The link between blood pressure and the amount of excreted sodium in a time unit is known as a pressure natriuresis. It plays a role in blood pressure regulation. On the other hand there is the autoregulation of kidney blood flow and the stability of glomerular filtration rate even at the face of variable blood pressure values. The authors try to explain the cooperation of these two separate mechanisms.
The experimental data show that different areas of intrarenal vessels act in distinct way. The cortical blood flow is much more under the autoregulation control mechanism than the medullar part. The elevated blood flow is observed in areas of decreased flow (the recruitment of flow), so even small and short-term blood pressure changes affect natriuresis, which determines the short and long-term blood pressure regulation. The partial oxygen pressure which is several times lower in the internal medullar part, plays the crucial role in microcirculation regulation. Even small hypoxia may affect and destroy these kidney structures. The nitric oxide plays an important role in microcirculation regulation also. There are experimental data suggesting that nitric oxide depletion is responsible for renal hypoperfusion and promotion of inflammatory response chich has effects in microcirculation dysfunction and sodium-sensitivity. Uric acid is another factor which causes hypertension and organ damage, promotes inflammation process in sodium-sensitive kidneys. The increased fructose consumption is one of the most important reasons of hyperuricemia.
Arterial Hypertension 2011, vol. 15, no 3, pages 143–154.