Macula densa
1: Glomerulus
2: Distal tubule
( HE staining , 100x)
As macula densa ( "tight spot") refers to cells of the straight part of the distal tubule ( 'pars recta') in Tubulussystems the kidney that the feeding blood vessel ( afferent ) of the renal corpuscle rest. In this area the tubular cells become highly prismatic and narrow. This leads to the fact that the cell nuclei of the individual cells are closer to one another, so that this area appears darker in the light microscopic specimen after the histological staining (hence the name "dense spot").
The macula densa is part of the juxtaglomerular apparatus of the kidney and is a chemoreceptor . He used to determine the sodium - and chloride - ion - concentration gradient between the blood in the afferent and the urine in the tubule.
The anatomist Karl Peter (1870–1955) first described the macula densa in 1908.
mechanism
Glomerular feedback
The cells of the macula densa have an ion transporter (Na + / K + / 2Cl- - symporter). This transport system transports ions that are located in the lumen of the distal tubule into the cells of the macula densa and thus measures the ion concentration, in particular the sodium and chloride concentration, in the urine. This measurement takes place indirectly via the speed of the transport. At high ion concentrations, i.e. hyperosmolar urine, adenosine is secreted from the cells of the macula densa, which leads to the contraction of the smooth muscles in the vas afferens. The afferent vessel narrows and the glomerular filtration rate (GFR) decreases. As a result, the flow of urine through Henle's loop decreases, so that more ions can be reabsorbed and the ion concentration in the distal tubule decreases. The opposite effect occurs with hypoosmolar urine.
Renin secretion
If hypoosmolar urine is measured at the chemoreceptors of the macula densa, this leads to a release of renin from the granular cells of the glomerular arterioles into the circulating blood and thus into the body. Renin is an enzyme which splits off the decapeptide angiotensin I from the prohormone angiotensinogen . Angiotensin I is cleaved by another peptidase, angiotensin converting enzyme (ACE), to form the octapeptide angiotensin II. Angiotensin II has a strong vasoconstrictor effect (“vasoconstrictive”) and leads to a systemic increase in blood pressure. In the kidney, it is primarily the efferent (behind the glomerulus) vessel that is narrowed. The pressure in the glomerulus increases and with it the GFR and the amount of primary urine formed.
See also
literature
- Aktories, Förstermann, Hoffmann, Starke General and special pharmacology and toxicology 9th edition Elsevierverlag ISBN 978-3-437-44490-6
- G. Heldmaier / G. Neuweiler Comparative Animal Physiology, Volume 2 - Vegetative Physiology . Berlin 2003, ISBN 978-3-540-21909-5 , p. 376
Individual evidence
- ↑ Wolfram F. Neiss: On the genesis of the 'Investigations on the structure and development of the kidney' (1909): A handwriting from Karl Peters to Philipp Stöhr senior In: Würzburger medical history reports 6. 1988, pp. 293-300; here: p. 293
- ↑ Karl Peter: About the finer structure of the human kidney. In: Negotiations of the Anatomical Society 22, 1908, pp. 159–163