• 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 (which we discuss in detail, elsewhere).

Myogenic mechanism:

• 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 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.