Factors Affecting Renal Blood Flow

Factors affecting renal blood flow 1) Renal/vascular geometry  This refers to perfusion pressure as well as afferent/efferent tone (the latter being a myogenic response)  A change in arteriolar resistance produces the same effect on renal blood flow regardless of whether this occurs in the afferent arteriole or efferent arteriole. Because these vessels are in series, a change in either one has the same effect on the total. When the two resistances both change in the same direction, their effects on the renal blood flow will be additive 2) Renal sympathetic nerve activity  Essentially all the blood vessels of the kidneys, including the afferent and the efferent arterioles, are richly innervated by sympathetic nerve fibres. Strong activation of the renal sympathetic nerves can constrict the renal arterioles and decrease renal blood flow 3) Autoregulation  This refers to the tendency of RBF to stay relatively constant when blood pressure changes  Its intrinsic mechanisms include the myogenic reflex and tubuloglomerular feedback 4) Tubuloglomerular feedback  As the filtration rate in an individual nephron increases or decreases, amount of sodium that escapes reabsorption in the proximal tubule and loop of Henle also increases or decreases. More sodium filtered means more sodium remaining in the lumen of the nephron and more sodium flowing from the thick ascending limb into distal tubule. The macula densa cells sense the amount of sodium and chloride in the lumen. In response to changing levels of luminal sodium chloride, it increases or decreases the secretion of transmitter agents into the interstitial space that affect the filtration in nearby glomerulus. (High levels of sodium flowing past the macula densa cause a decrease in filtration rate; low levels of sodium flowing past cause a higher filtration rate). This is achieved as the transmitter agents released by the salt-sensing macula densa cells produce vasoconstriction of the afferent arteriole, thereby reducing hydrostatic pressure in glomerular capillaries. These same agents also produce contraction of glomerular mesangial cells, thereby reducing the effective filtration coefficient. o Example: An increase in arterial pressure leads to increases in glomerular capillary pressure, RPF, and GFR. The increase in GFR leads to an increased delivery of Na+, Cl-, and fluid into the proximal tubule and, ultimately, to the macula densa cells of the juxtaglomerular apparatus. Because of high Na/K/Cl co-transporter activity at the apical membrane of the macula densa cell, increases in luminal [Na+] and [Cl-] translate to parallel increases in intracellular concentrations of these two ions. The result is an increase in [Ca2+]i that causes the macula densa cell to release paracrine agents (ATP, adenosine, thromboxane, or other substances) that trigger a contraction of nearby vascular smooth muscle cells. Net effect is increase in afferent arteriolar resistance and decrease in GFR, thereby counteracting the initial increase in GFR. 5) Hormones/Local factors     Hormones that constrict afferent and efferent arterioles, causing reductions in GFR and renal blood flow, include norepinephrine and epinephrine Angiotensin II preferentially constricts efferent arterioles, increased angiotensin II levels will raise glomerular hydrostatic pressure while reducing renal blood flow Atrial Natriuretic Peptide (ANP) works to supress the sympathetic nervous system as well as RAAS. Thus, it works to increase GFR and, in doing so, urination. It prevents any excessive Na+ and H2O overload Hormones and autacoids that cause vasodilation and increased renal blood flow and GFR include the prostaglandins (PGE2 and PGI2) and bradykinin. By opposing vasoconstriction of afferent arterioles, the prostaglandins may help prevent excessive reductions in GFR and renal blood flow. (Administration of NSAIDs / inhibit prostaglandin synthesis may cause reductions in GFR)