BP and renal blood flow influence GFR GFR is remarkably constant over a wide range of BPs (mean arterial BP 80 ? 180 mm Hg) Increase resistance in afferent arteriole decrease hydrostatic pressure on glom side of constriction decrease in GFR Decrease ? increase ? increase GFR Increase resistance in efferent arteriole blood ?dams up? in front of constriction increase hydrostatic pressure in glom capillaries increase GFR Decrease ? decrease ? decrease GFR GFR is subject to autoregulation Myogenic response ? intrinsic ability of vascular smooth muscle to respond to pressure changes; tonic level of arteriolar contraction when BP is high, disappears if BP decreases when mean BP drops < 80 mm Hg, GFR decreases Tubuloglomerular feedback ? paracrine signaling mechism through which changes in blood flow through loop of Henle influences GFR (1) GFR increases (2) flow through tubule increases (3) flow past macular densa increases (4) paracrine diffuses from macula densa to afferent arteriole (5) afferent arteriole constricts resistance in afferent arteriole increase hydrostatic pressure in glomerulus decreases GFR decreases Macular densa ? plaque of cells that transport NaCl and possibly pass several paracrine signals through arteriole Granular cells ? specialized smooth muscle cells that secret rennin, enzyme involved in salt and H2O balance Hormones and autonomic neurons also influence GFR Mediated by sympathetic neurons that innervate both afferent and efferent arterioles Sym innervation of alpha neurons vasoconstriction Little effect on GFR if moderate But if BP drops sharply (i.e. hemorrhage, severe dehydration) sym induced vasoconstriction of arterioles decreases GFR & renal blood flow conserve vol Angiotnesin II ? potent vasoconstrictor Prostaglandins ? vasodilators Hormones acting on podocytes ? change size of filtration slits Widen more SA for filtration increase GFR Contraction less SA for filtration decrease GFR
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