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BIOL 1119 (84)
Lecture 32

BIOL 1119 Lecture 32: Class 32
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Department
Biology
Course
BIOL 1119
Professor
Christopher Richardson
Semester
Spring

Description
Class 32 Control of GFR GFR: the amount of filtrate formed per minute by both kidneys. Only small portion of this filtrate is actually eliminated as urine - Must be precisely controlled to ensure proper filtration and reabsorption - Is adjusted by changing glomerular blood pressure - Controlled to ensure proper filtration and reabsorption o Renal autoregulation: 2 important mechanisms (local level – nephron) o Sympathetic control (many nephrons at once) o Hormonal mechanism: renin and angiotensin (BP) - Analogy: o Water balloon with tiny holes: analogy of glomerular BP o Squeeze balloon and water pressure inside will build – water squirt out faster o Pressure building in glomerulus – cause water filter out at a faster rate o Constrict afferent arteriole and/or dilate efferent arteriole – decrease pressure in glom,- decrease GFR o In general: dilate afferent arteriole and/or constrict efferent arteriole – increase pressure in glom – increase GFR – increase BP Renal Autoregulation - The ability of nephrons to adjust their own blood flow and GFR locally without external control - Use auto regulation to maintain relatively stable GFR even if BP changes o Myogenic mechanism the tendency of smooth muscle to contract when stretched ▪ Responds to immediate pressure changes at entrance to glomerulus to maintain the same pressure inside glom ▪ Goal: keep GFR constant w/ BP fluctuations ▪ Increase local BP = stretches AA (snap back when stretched), AA constricts in response • Increase resistance to oppose increased BP at entrance of glom o Lowers net BP and net flow in glom back down to normal o Systemic BP – local R = net local BP entering glom ▪ Decrease local BP = less stretch of AA, AA dilates in response • Decrease resistance in response to decreased BP at entrance of glom • Increase net local BP and increase net flow into glom back up to normal • Systemic/local BP into glom – local R = net BP entering glom o Tubuloglomerular feedback: several structures at end of nephron loop ▪ Mechanism localized to whole nephron by which the glom receives feedback on the downstream tubular fluid flow rate ▪ Involves a set of structures called the juxtaglomerular (JG) apparatus where the ascending limb of the nephron loop passes b/t the AA and EA ▪ 3 types of special cells are found in JG apparatus • JG cells are enlarged smooth muscle cells found mostly in the AA (not part of wall) – w/ few in the EA across from mascula densa o Dilate and constrict arterioles and in response to a BP drop will release renin • Mascula densa is a patch of slender epithelial cells on the side of the tubule facing the arterioles at the end of the nephron loop o In contact w/ fluid, act as sensors o Detects variations in fluid flow and composition of tubular fluid o Secretes paracrine chemical messengers that stimulate JG cells • Mesangial cells are in the gaps b/t AA and EA and among capillaries of the glom o Connected to and communicate with mascular densa and JG cells – through gap junctions and paracrine secretions JG Apparatus o Systemic BP is not changing during TG feedback unlike the myogenic mechanism ▪ Pressure into glom constant, if P constant then increase R to decrease F (P/R = F) o Mascula densa detects sodium levels in tubular fluid flowing past it ▪ Flow decreases, decrease NA, changes w/ diet ▪ Low GFR causes low tubular flow rate in DCT: brings less sodium past mascula densa: detects as low flow • Mascula densa rele
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