RENAL SYSTEM
Renal Lecture 7 Dr. Janan AlrefaeeThree factors preserve hyperosmolarity of the renal medulla interstitial fluid 1-The large amounts of water are reabsorbed into the cortex, rather than into the renal medulla. 2- Countercurrent exchange in the vasa recta 3-The medullary blood flow is low.
1-The large amounts of water are reabsorbed into the cortex, rather than into the renal medulla. The tubular fluid enters the distal convoluted tubule in the renal cortex with osmolarity about 100 mOsm/L, then large amounts of water are reabsorbed from the cortical collecting tubule, when there is a high concentration of ADH, into the cortex interstitium (few amount into medulla interstitum).
The reabsorbed water is quickly carried away by the vasa recta into the venous blood. So the fluid at the end of the collecting ducts has the same osmolarity as the interstitial fluid of the renal medulla—about 1200 mOsm/L.
2-Countercurrent exchange in the vasa recta The vasa recta serve as countercurrent exchangers, minimizing washout of solutes from the medullary interstitium out to the circulation. In which Plasma flowing down the descending limb of the vasa recta becomes more hyperosmotic up to 1200 at its tip because of diffusion of water out of the blood and diffusion of solutes from the renal interstitial fluid into the blood due to medulla hyperosmolarity.
In the ascending limb of the vasa recta, solutes diffuse back into the interstitial fluid and water diffuses back into the vasa recta. Thus the solute will recycle in the medulla without loss while the water bypasses it. Without the U shape of the vasa recta capillaries, large amounts of solutes would be lost from the renal medulla.
3. The medullary blood flow is low: It is less than 5 % of the total renal blood flow, so it minimizes solute loss from the medullary interstitium but it is sufficient for tissues metabolic needs.* Increased medullary blood flow by vasodilators or increases in arterial pressure, lead to wash out some of the solutes from the renal medulla and reduce urine concentrating ability.
Changes in osmolarity of the tubular fluid
Disorders of urinary concentrating ability 1. Inappropriate secretion of ADH (central” diabetes insipidus). 2. Impairment of the countercurrent mechanism. 3. Inability of the distal tubule, collecting tubule, and collecting ducts to respond to ADH (“Nephrogenic” Diabetes Insipidus).
Renal mechanisms for excreting dilute urine (large amount, with osmolarity as low as 50 mOsm/L): this achieved by reabsorbing solutes to a greater extent than water, but this occurs only in certain segments of the tubular system as follows. 1. Normally, fluid leaving the ascending loop of Henle and early distal tubule is always dilute (100 mOsm/L), regardless ADH level. 2. Tubular fluid in distal and collecting tubules is diluted and it becomes further diluted in the absence of ADH.
Osmolar clearance It is the volume of plasma cleared of solutes each minute & it is calculated: Cosm=Uosm X V/Posm Where Uosm is the urine osmolarity, V is the urine flow rate, and Posm is the plasma osmolarity. CH2O=V-Cosm
When free-water clearance is positive, excess water is being excreted by the kidneys; when free-water clearance is negative, excess solutes are being removed from the blood by the kidneys and water is being conserved. Whenever urine osmolarity is greater than plasma osmolarity, free-water clearance will be negative, indicating water conservation.
Control of extracellular fluid osmolarity and sodium concentration Normal plasma sodium concentration average concentration is of about 142 mEq/L & osmolarity averages about 300 mOsm/L. As sodium and its associated anions account for about 94 % of the solute in the extracellular compartment.
Plasma osmolarity (Posm) can be roughly approximated as: Posm = 2.1 *Plasma sodium concentration To be more exact, especially in conditions associated with renal disease, the contribution of two other solutes, glucose and urea, should be included (glucose and urea contributing about 3 to 5 per cent of the total osmoles).
Two systems regulate the sodium concentration and osmolarity of extracellular fluid: The osmoreceptor-ADH system. The thirst mechanism.
1- Osmoreceptor-ADH Feedback System When osmolarity (plasma sodium concentration) increases above normal due to water deficit, for example, rapidly this feedback system operates as follows: 1- This cause osmoreceptor nerve cells, which located in the anterior hypothalamus near the supraoptic nuclei, to shrink.
2- This shrink causes them to fire, sending nerve signals to nerve cells in the supraoptic nuclei and paraventricular nuclei (that synthesize ADH), which then spread these signals down the stalk of the pituitary gland to the posterior pituitary. 3. This action potentials stimulate the release of ADH, which is stored in secretory granules (or vesicles) in the nerve endings.
4. ADH enters the blood stream and is transported to the kidneys, where it increases the water permeability of the late distal tubules, cortical collecting tubules, and medullary collecting ducts and this lead to: 5. Increase water reabsorption and excretion of a small volume of concentrated urine. ●The opposite sequence of events occurs when the extracellular fluid becomes too dilute (hypo-osmotic).
●ADH release is also controlled by cardiovascular reflexes that respond to decreases in blood pressure and/or blood volume including (1) the arterial baroreceptor reflexes and (2) the cardiopulmonary reflexes. These reflexes go to the hypothalamic nuclei that control ADH synthesis and secretion.