BSC 1086C Lecture 16: Chapter 28 pt. 2

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Biological Sciences
BSC 1086C

Glomerular Filtration - Passive mechanical process driven by hydrostatic pressure - The glomerulus is very efficient filter because o Its filtration membrane is very permeable and it has a large surface area o Glomerular blood pressure is higher (e.g plasma proteins) and function to maintain colloid osmotic pressure of the blood Glomerular Filtration Rate (GFR) - Volume of filtrate formed per minute by the kidneys (120-125 ml/min) - Governed by (and directly proportional to) o Total surface area available for filtration o Filtration membrane permeability o NFP Regulation of Glomerular filtration - GFR is tightly controlled by two types of mechanisms o Intrinsic controls (renal autoregulation) act locally within the kidney o Extrinsic controls- Nervous and endocrine mechanisms that maintain blood pressure, but affect kidney function Intrinsic Controls - Maintains a nearly constant GFR when MAP is in the range of 80-180 mm HG - Two types of renal autoregulation o Myogenic mechanism o Tubuloglomerular feedback mechanism, which senses changes in the juxtaglomerular apparatus Myogenic Mechanism - Increase BP -> constriction of afferent arterioles o Helps maintain normal GFR o Protects glomeruli from damaging high BP - Decrease BP -> dilation of afferent arterioles o Helps maintain normal GFR Tubuloglomerular Feedback Mechanism - If GFR increases, filtrate flow rate increases in the tubule - Filtrate NaCl concentration will be high because of insufficient time for reabsorption - Macula densa cells of the JGA respond to increase NaCl by releasing a vasoconstricting chemical that acts on the afferent arteriole -> decrease GFR - The opposite occurs if GFR decrease Extrinsic Controls - Sympathetic Nervous System o Under normal conditions at rest ▪ Renal blood vessels are dilated ▪ Renal autoregulation mechanisms prevail o Under extreme stress ▪ Norepinephrine is released by the sympathetic nervous system ▪ Epinephrine is released by the adrenal medulla ▪ Both cause constriction of afferent arterioles, inhibiting filtration and triggering the release of renin - Renin-Angiotensin Mechanism o Triggered when the granular cells of the JGA release renin Effects of Angiotensin II - Constricts arteriolar smooth muscle, causing MAP to rise - Stimulates the reabsorption of Na+ - Stimulates the hypothalamus to release ADH and activates the thirst center - Constricts efferent arterioles, decreasing peritubular capillary hydrostatic pressure and increasing fluid reabsorption - Causes glomerular mesangial cells to contract, decreasing the surface area available for filtration Tubular Reabsorption - A selective transepithelial process o All organic nutrients are reabsorbed o Total water and ion reabsorption are hormonally regulated o Included active and passive process o Two routes ▪ Transcellular ▪ Paracellular: Limited to water movement and reabsorption of Ca2+, Mg2+, K+, and some Na+ in the PCT where tight junctions are leaky Active and Passive Reabsorption - Sodium reabsorption is a primary active process using Na+-K+ ATPases (sodium-potassium pumps_ in the basolateral membrane of tubule cells - Na+ passes in through the luminal membrane by secondary active transport or facilitated diffusion mechanisms - Concentration gradient for Na+ also provides the energy and the means for reabsorbing organic nutrients, such as glucose and amino acids, via secondary active transport Reabsorption of Nutrients, Water, and Ions - Organic nutrients are reabsorbed by secondary active transport o Transport maximum (Tm) reflects the number of carriers in the renal tubules
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