Glomerular Filtration
Glomerular filtration is the permeation of water and certain solutes in the blood from “the capillaries of the glomerulus” to the “capsular region of the nephron” (Saladin, 2021, p. 875). According to Ogobuiro and Tuma (2023), this is a passive process that requires no energy—hydrostatic pressure pushes the filtrate (solutes and water) across the filtration membrane. Notably, the total filtrate both kidneys produce in a minute is called the glomerular filtration rate (GFR). GFR is determined by multiplying the net filtration pressure (NFP) and the filtration coefficient (Kf).
Kf is the amount of filtrate produced in every 1 mm Hg of net filtration pressure. In male adults, Kf is approximately 12.5 mL and about 10% lower in women (Saladin, 2021). Given that NFP is 10 mm Hgout, the GFR in males would be 125 mL/min.
GFR is mainly regulated by changing glomerular blood pressure. This is achieved through intrinsic and extrinsic mechanisms. Intrinsic regulation occurs through renal autoregulation, a mechanism where nephrons adjust their own blood flow via the myogenic and tubuloglomerular feedback mechanisms. Myogenic action contracts afferent arterioles to prevent blood flow when blood pressure rises, and in low blood pressure, it relaxes the afferent arterioles for more blood flow.
Further, tubuloglomerular feedback involves macula densa, sensory cells that sense sodium chloride (NaCl). High blood pressure and high GFR prevent more Na reabsorption, resulting in high Na levels. Subsequently, when the macula densa cells sense a high sodium level, they release vasoconstricting chemicals that contract the afferent arterioles, reducing blood flow. Conversely, in low blood pressure, sodium concentration is low due to increased sodium reabsorption; therefore, the macula densa cells do not release vasoconstrictor chemicals (Ogobuiro & Tuma, 2023).
Extrinsic mechanisms regulate GFR via sympathetic and renin-angiotensin-aldosterone mechanisms. In sympathetic regulation, a significant decrease in the fluid volume in the extracellular causes the secretion of norepinephrine and epinephrine that vasoconstrict the afferent arterioles, decreasing the blood flowing to the kidneys and, in turn, the GFR (Ogobuiro & Tuma, 2023).
The renin-angiotensin-aldosterone mechanism is activated when blood pressure falls, triggering the release of renin, which is converted to angiotensin II hormone. Angiotensin II maintains blood pressure in several ways. For instance, it constricts the efferent arterioles more strongly than the afferent arteriole, consequently elevating blood pressure in the glomerulus and, hence, GFR.
References
Ogobuiro, I., & Tuma, F. (2023, July 24). Physiology, renal. StatPearls – NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK538339/
Saladin, K. (2021). Anatomy and physiology: The unity of form and function (9th ed.). McGraw-Hill Education.
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