RENAL SYSTEM
Renal Lecture 5 Dr. Janan AlrefaeePeritubular capillary and renal interstitial fluid physical forces *Normally more than 99 % of the water and solutes are reabsorbed from tubule lumen to interstitium and then to the peritubular capillaries. *Increase peritubular capillary reabsorption, increase reabsorption from the renal tubules and vice versa. This is by changing physical forces (hydrostatic and colloid osmotic pressures) in the renal interstitium surrounding the tubules.
*The normal peritubular capillary reabsorption rate is about 124 ml/min, which is calculated as: Reabsorption = Kf * Net reabsorptive force =12.4*10=124 ml/min
This normal high rate of peritubular capillaries fluid reabsorption (124 ml/min) due to: First: The net reabsorptive force about 10 mm Hg favors reabsorption into the peritubular capillaries which represents the sum of the forces include (1) peritubular capillary hydrostatic pressure [Pc]( 13 mm Hg) and colloid osmotic pressure of the proteins in the renal interstitium (πif) (15 mm Hg) both opposes reabsorption. (2) Hydrostatic pressure in the renal interstitium (Pif) (6 mm Hg) and colloid osmotic pressure of the peritubular capillary plasma proteins (πc) (32 mm Hg),both favors reabsorption.
Second: the large filtration coefficient (Kf) (12.4 ml/min/mm Hg) is due to the high hydraulic conductivity and large surface area of the capillaries.
Regulation of tubular reabsorption by: 1-Glomerulotubular Balance It is the intrinsic ability of the tubules to increase their reabsorption rate with constant % in response to increased tubular load (increase GFR), this balance occurs in proximal tubules and less in loop of henle. {e.g. if GFR increase from 125 to 150 ml/min, the rate of proximal tubular reabsorption also increase from about 81 to about 97.5 ml/min ( both 65 % of GFR)}. The glomerulotubular balance prevents overloading of the distal tubular segments when GFR increases and it is a second line of defense to buffer the effects of spontaneous GFR changes on urine output.
2-Peritubular capillary and renal interstitial fluid physical forces First, the peritubular capillary hydrostatic pressure (oppose reabsorption) which is influenced by (1) the arterial pressure (+ve relation) and (2) resistances of the afferent and efferent arterioles (-ve relation).
Second, the peritubular capillarie colloid osmotic pressure (favour reabsorption) which is determined by (1) the systemic plasma colloid osmotic pressure (+relation) and (2) the filtration fraction (+relation). * Kf has + ve relation with the reabsorption rate but it remains relatively constant in most physiologic conditions.
3-Effect of arterial pressure on urine output—the pressure-natriuresis and pressure-diuresis mechanisms Even small increases in arterial pressure lead to increase urinary excretion of sodium and water, phenomena that are referred to as pressure natriuresis and pressure diuresis, these contribute to several factors:
1- A slight increase in GFR (autoregulation). 2- An increases the peritubular capillary pressure, a decrease in tubular reabsorption % of sodium and water due to increases the peritubular capillary hydrostatic pressure and subsequent increase in the renal interstitial fluid hydrostatic pressure. 3-A reduced angiotensin II formation, decreased tubular sodium reabsorption (discussed later).
4-Hormonal control of tubular reabsorption First- Aldosterone: by its action on the principal cells increases sodium reabsorption and potassium secretion is by stimulating the sodium-potassium ATPase pump.
Second- Angiotensin II Angiotensin II increases sodium and water reabsorption from the renal tubules through three main effects: 1. It stimulates aldosterone secretion. 2. It constricts the efferent arterioles leading to reduce peritubular capillary hydrostatic pressure & increases the concentration of proteins and the colloid osmotic pressure in the peritubular capillaries; both raise sodium and water reabsorption.
3. It directly stimulates sodium reabsorption in the proximal tubules, the loops of Henle, the distal tubules, and the collecting tubules by stimulating sodium-potassium ATPase pump on the tubular epithelial cell basolateral membrane and stimulating sodium-hydrogen exchange in the luminal membrane, especially in the proximal tubule.
Third-ADH: it increases the water permeability of the distal tubule, collecting tubule, and collecting duct epithelia conserving water in dehydration. Forth-Atrial Natriuretic Peptide: Specific cells of the cardiac atria, when distended because of plasma volume expansion, secrete a peptide called atrial natriuretic peptide which inhibit the reabsorption of sodium and water by the renal tubules, especially in the collecting ducts and increases urinary excretion, which helps to return blood volume back toward normal.
Fifth-Parathyroid Hormone It increases calcium reabsorption by distal tubules and loops of Henle. It also inhibits phosphate reabsorption by the proximal tubule and stimulates magnesium reabsorption by the loop of Henle.
4-Sympathetic Nervous System Activation: It decreases sodium and water excretion by: first- constricting renal arterioles, thus reducing GFR. Second- increasing sodium reabsorption in proximal tubule, thick ascending limb of the loop of Henle, and perhaps in more distal parts of the renal tubule. Third- increasing renin release.