Intrinsic Mechanisms of GFR Regulation

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Intrinsic Mechanisms of GFR Regulation 1
Intrinsic Mechanisms of GFR 
Regulation
Class Fisiologia Renal
Created
Reviewed
Overview
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
Physiological responses that are initiated by renal structures to modify the 
hydrostatic capillary pressures; renal autoregulation 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.
Myogenic mechanism:
Jan 3, 2021 921 PM
Intrinsic Mechanisms of GFR Regulation 2
Relies on inherent properties of the arterioles, themselves.
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:
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 tubule senses the high salt concentration in the 
ultrafiltrate as it passes through the distal tubule and in response, it 
releases vasoconstrictor chemicals.
Consequently, the nearby afferent arteriole constricts, which, 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.
Intrinsic Mechanisms of GFR Regulation 3