Regulation of glomerular filtration
Glomerular filtration rate is regulated by both intrinsic and extrinsic controls. These two types of controls serve two different (and sometimes opposing) needs. The kidneys need a relatively constant glomerular filtration rate in order to do their job and maintain extracellular homeostasis. On the other hand,the body as the whole needs a constant blood pressure, and therefore a constant blood volume.
Intrinsic controls (renal autoregulation) act locally within the kidney to maintain glomerular filtration rate, while extrinsic controls by the nervous and endocrine systems maintain blood pressure. In extreme changes of blood pressure (mean arterial pressure less than 80 or greater than 180 mmHg), extrinsic control take precedence over intrinsic controls.
INTRINSIC CONTROLS (RENAL AUTOREGULATION)
By adjusting its own resistance to blood flow, a process called renal autoregulation, the kidney can maintain a nearly constant glomerular filtration rate despite fluctuations in systemic arterial pressure. Renal autoregulation entails two types of controls :
- Myogenic mechanism
The myogenic mechanism reflects the tendency of vascular smooth muscle to contract when stretched. Increasing systemic blood pressure causes the afferent arterioles to constrict, which restricts blood flow into the glomerulus and prevents glomerular blood pressure from rising to damaging levels. Declining systemic blood pressure causes dilatation of afferent arterioles and raises glomerular hydrostatic pressure. Both responses help maintain a normal glomerular filtration rates.
- Tubuloglomerular feedback mechanism
Autoregulation by the flow-dependent tubuloglomerular feedback mechanism is “directed” by the macula densa cells of the juxtaglomerular apparatus. These cells, located in the walls of the ascending limb of Henle’s loop, respond to filtrate NaCl concentration (which varies directly with filtrate flow rate). When glomerular filtration rate increases, there is insufficient time for reabsorption and the concentration of NaCl in the filtrate remains high. This causes the macula densa cells to release a vasoconstrictor chemical (probably ATP) that causes intense constriction of the afferent arteriole. This constriction hinders blood flow into the glomerulus, which decreases the net filtration pressure and glomerulus filtration rate, allowing more time for filtrate processing (NaCl reabsorption),
On the other hand, when macula densa cells are exposed to slowly flowing filtrate with its low NaCl concentration, ATP release is inhibited, causing vasodilatation of the afferent arterioles. This allows more blood to flow into the glomerulus, thus increasing net filtration presure and glomerulus filtration rate.
Autoregulatory mechanism maintain a relatively constant glomerulus filtration rate over an arterial pressure range from about 80 to 180 mmHg. Consequently, our normal day to day activity (such as exercise, sleep or changes in posture) do not cause large changes in water and solute excretion. However, the intrinsic controls cannot handle extremely low systemic blood pressure, such as might result from serious hemorrhage (hypovolemic shock). Once the mean arterial pressure drops below 80 mmHg, autoregulation ceases.