Renal Blood Flow and Regulation Tutorial 1 PDF

Physiology Faculty of medicine RAU-213 Module Tutorial 1 Renal blood flow and its regulation Staff members of Medical Physiology After studying this section, you should be able to: Define renal blood flow (RBF), renal plasma flow (RPF), renal fraction and filtration fracti...

Physiology Faculty of medicine RAU-213 Module Tutorial 1 Renal blood flow and its regulation Staff members of Medical Physiology After studying this section, you should be able to: Define renal blood flow (RBF), renal plasma flow (RPF), renal fraction and filtration fraction and give normal values. Identify auto regulation of RBF Recognize the mechanisms of auto regulation. Demonstrate the sympathetic nervous system influence on RBF? Points out hormones regulating renal blood flow?  It is about 20% of the C.O.P (1200 ml/min). Renal blood flow to different parts of the kidney differs according to their functions. It is highest in the cortex (4 – 5 ml /gm tissue / min) to allow high rate of filtration by the glomeruli , but it is very low in the inner medulla (0.2 – 0.25 ml / gm tissue / min) to help maintenance of hyperosmolar environment (through vasa recta) in that region (help in formation of concentrated urine). This high renal blood flow is necessary for the high GFR.  Renal blood flow Regulation Nervous Hormonal Autoregulation 1- Nervous ( sympathetic ) regulation: (a) Mild to moderate sympathetic stimulation has a little or no effect on renal blood flow and GFR (due to autoregulation). (b) Strong sympathetic stimulation leads to more afferent arteriole constriction leading to decreased GFR and renal blood flow. 2-Hormonal and autacoidal control of GFR and renal blood flow: Vasoconstrictor hormones: -Adrenaline. -Noradrenaline. -Endothelin. -These hormones cause V.C of afferent and efferent arterioles leading to decreased renal blood flow and GFR. -Angiotensin II : -It has a selective V.C on efferent arterioles leading to increased glomerular hydrostatic pressure and decreased peritubular capillary pressure. So GFR increases and tubular reabsorption increases. But it decreases renal blood flow. N.B: -Drugs that antagonize angiotensin II (angiotensin converting enzyme inhibitors (AC inhibitors) leads to significant reduction in GFR. -Angiotensin II secreted in conditions associated with decrease in ABP which tend to decrease GFR, so Angiotensin II tend to prevent the decrease of GFR.  Vasodilator hormones: ʘ Nitric Oxide (N.O) and Prostaglandins. ʘ Both have V.D action on renal arterioles leading to increased renal blood flow and GFR N.B: diseases that cause damage of normal endothelium, lead to hypertension. ʘ These hormones antagonize the V.C agents so keeping GFR, sodium and water excretion at a normal level. ʘ Drugs which inhibit prostaglandins synthesis e.g. aspirin and non-steroidal anti- inflammatory drugs leads to significant reduction of GFR. ʘ The balance between vasoconstrictors and vasodilators keep the GFR at a normal level. 3-Autoregulation of renal blood flow: Definition: It is an intrinsic feedback mechanism by which the kidney keeps renal blood flow and GFR constant despite marked changes in systemic arterial blood pressure. Range: it works in ABP range 70-170 mmHg. The importance: of the autoregulatory mechanism is to prevent marked changes in GFR, sodium and water excretion in spite of changes in systemic A.B.P Example: If mean systemic arterial blood pressure is increased by 25 %, without auto regulation GFR increases by 25 % i.e from 180 L / day to 225 L / day and urine excretion increases by 225 – 180 = 46 liters / day leading to death due to rapid loss of body water. Autoregulation prevent occurrence of such conditions by 2 mechanisms A-Tubulo-glomerular feedback mechanism. B-Myogenic Mechanism. A-Tubulo – glomerular feedback mechanism: -It provides a link between sodium chloride concentration at macula densa with the control of renal vascular resistance. -It depends on the activity of juxta- glomerular apparatus. -Decreased NaCl load in the distal convoluted tubules the macula densa stimulates two mechanisms: a-Afferent arteriolar feedback mechanism. b-Efferent arteriolar feed back mechanism. a-Afferent arteriolar feedback mechanism: -As impulses from macula densa leads to V.D of afferent arterioles leading to increased renal blood flow, glomerular hydrostatic pressure leading to increased GFR so NaCl load in distal tubules is increased. -This is mediated by PGI2. b-Efferent arteriolar feed back mechanism: -As macula densa stimulate juxta –glomerular cells to secrete rennin leading to formation of angiotensin II, which leads to V.C of efferent arterioles leading to: 1-Increased glomerular hydrostatic pressure leading to increased GFR and Na cl load at distal tubules. 2-Decreased peritubular capillary pressure leading to increased rate of tubular absorption and increased body water and solutes.  Rennin hormone Causes of release: Sympathetic stimulation of juxta –glomerular cells (β1-adrenoceptors). decreased sodium delivery to the distal tubules of the kidney. Decrease renal blood flow. Function: It acts upon a circulating angiotensinogen to form angiotensin I, which is converted to angiotensin II by angiotensin converting enzyme (ACE). B- Myogenic mechanism: -It's inherent property. -Increased arterial blood pressure or renal blood flow leads to stimulation of stretch receptors in the afferent arterioles leading to reflex V.C of the arterioles, So decreasing the effect of high blood pressure on RBF and GFR to normal and vice versa. - Stretch of the vascular wall increases Ca ions movement from Ext. cellular fluid to cells causing its contraction. N.B: there are other factors increase renal blood flow and GFR like high protein diet and hyperglycemia.  Oxford Handbook of Medical Sciences ,third edition 2021, Robert Wilkins, Simon Cross, Ian Megson, David Meredith, OXFORD university press. (Handbook) Lippincott Illustrated Reviews: Integrated Systems. Sandra K. Leeper-Woodford, MS, Macon, Georgia Linda R. Adkison, MS Copyright © 2015 Wolters Kluwer. (Student book) Guyton and Hall Textbook of Medical Physiology 14th edition John E. Hall, PhD and Michael E. Hall, MD, MS. Copyright © 2021 by Elsevier, Inc. All rights reserved http://evolve.elsevier.com/Hall/physiology/ (Text book)