Intrinsic Mechanisms of GFR Regulation
Glomerular filtration rate (GFR) is the total volume of ultrafiltrate formed by the collective kidney nephrons per minute;
GFR is closely regulated to balance potentially opposing requirements:
– Excess solutes and water needs to be removed from the blood.
– The body tissues need nearly constant blood volume and pressure.
Intrinsic mechanisms are physiological responses that are initiated by renal structures to modify the hydrostatic capillary pressures; renal autoregulation.
They work to maintain nearly constant GFR as long as mean arterial pressure is 80-180 mmHg, which allows for consistent kidney functioning despite changes in blood pressure.
During daily activities, cardiac output, and, therefore, arterial blood pressure fluctuates—for example, during exercise it increases and during sleep it decreases.
At high blood pressures, autoregulation protects the glomerulus from damage, and, at lower blood pressures, it ensures that the kidneys receive sufficient blood flow to filter wastes.
If mean arterial pressure drops below 80 mmHg, such as during hemorrhage, extrinsic mechanisms activate (which we discuss in detail, elsewhere).
The myogenic mechanism relies on inherent properties of the
arterioles, themselves.
Recall that the arteriole walls comprise smooth muscle, made of vascular smooth muscle cells.
When increased renal blood flow exerts increased hydrostatic capillary pressure on the walls, stretch receptors are activated and induce vasoconstriction.
This reduces renal blood flow and, therefore, GFR.
When renal blood flow is low, the stretch receptors are inactivated, and the arteriole dilates to increase GFR.
Tubuloglomerular feedback mechanism
The tubuloglomerular feedback mechanism relies on interaction between the nephron tubule and glomerulus.
As renal blood flow increases, so does hydrostatic capillary pressure, and, therefore, GFR increases.
As the GFR increases, so does the concentration of salt in the ultrafiltrate, because high flow rate allows less time for tubular reabsorption.
The macula densa of distal tuble senses the high salt concentration in the ultrafiltrate as it passes through the distal tubule.
In response, it releases vasoconstrictor chemicals (the specifics of which are disputed).
Consequently, the nearby afferent arteriole constricts, which, as we saw earlier: Reduces renal blood flow, hydrostatic capillary pressure, and GFR.
When renal blood flow decreases, so does the sodium concentration, and eventually the macula densa stops releasing vasoconstrictors, which ultimately allows renal blood flow and GFR to again increase.
