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18.2). The ADH increases apical water channels, or aquaporins (in the principal cells, AQP-2), which allow only waterto be reabsorbed, effectively concentrating solutes in thetubular fluid, which at this point is considered urine.The urine-concentrating mechanism depends on the plasmalevel of ADH and the osmolar concentration of the interstitialfluid surrounding the collecting ducts.
Plasma ADH is tightlyregulated, and water channels are continually being insertedand removed from the apical membranes of the CD cells, tomaintain extracellular fluid balance through the regulatedretention and excretion of water in the urine. The abilityof the ADH to effectively promote water reabsorption isdependent on the medullary concentration gradient. ADHdependent urea recycling plays an important role in the abilityto concentrate urine, because the additional urea added to theIncreased urine output in response to expansion of plasmavolume entails both sodium excretion (natriuresis) and waterexcretion (diuresis).
The ability to excrete hypotonic urine isas important to fluid homeostasis as the ability to excreteconcentrated urine, and impairment of this mechanism canbe life-threatening (see exercise-induced hyponatremia). Theconcept of free water clearance is useful in quantifying waterexcretion during diuresis; it is defined as water excretionin excess of the water required for iso-osmotic excretionof the solutes present in the urine. Free water clearance isMicturition is the process of emptying the bladder (urination). Micturition is under voluntary control, becausethe external sphincter of the bladder is skeletal muscle.
However,the micturition reflex system is under both sympathetic andparasympathetic control. While the bladder is filling, the sympathetic nerves relax the smooth muscle of the bladder wall,accommodating the urine, and contract the internal urethralsphincter smooth muscle. When the bladder becomes “full,”mechanoreceptors signal a spinal reflex arc that stimulates parasympathetic contraction of the bladder (detrusor muscle) andrelaxation of internal sphincters. The external urethral sphincter is skeletal muscle, and is voluntarily relaxed, allowingurination.Renal PhysiologyMECHANISM OF ANTIDIURETIC HORMONE IN REGULATING URINE VOLUME AND CONCENTRATIONADH is produced in supraoptic and paraventricularnuclei of hypothalamus and descends along nervefibers to neurohypophysis, where it is stored forsubsequent release.Blood osmolality and volume are modified byfluid intake (oral or parenteral); water andelectrolyte exchange with tissues, normalor pathological (edema); loss via gut(vomiting, diarrhea); loss into bodycavities (ascites, effusion); orloss externally(hemorrhage,sweat).ADH release is increased by highblood osmolalityaffecting hypothalamicosmoreceptors and bylow blood volumeaffecting thoracic andcarotid volume receptors;low osmolality and high bloodvolume inhibit ADH release.H2OIn presence of ADH, blood flowto renal medulla is diminished,thus augmenting hypertonicity ofmedullary interstitium by minimizing depletion of solutes viabloodstream.H2OH2OADH causes walls of collecting ducts tobecome more permeable to water and thuspermits osmolar equilibration and absorptionof water into the hypertonic interstitium; asmall volume of highly concentrated urine isexcreted.H2OMaxMaxPlasma (ADH)H2OPlasma (ADH)2220310270290Plasma osmolality (mosm/kg H2O)0⫺30 ⫺20 ⫺10 0 10 20% Change in blood volume or pressureFigure 18.2 The Renal Response to ADH Secretion The scheme above illustrates the releaseand action of antidiuretic hormone (ADH).
In response to dehydration, ADH is secreted from the posteriorpituitary gland into the circulation. It acts on the kidneys to increase water channels in the collecting ducts,allowing solute-free water absorption, and also increases urea reabsorption in the medullary collecting ducts.The additional urea is added to the inner medullary interstitium and contributes to the high interstitial osmolarconcentration.Urine Concentration and Dilution Mechanisms223WATER, ION, AND UREA EXCHANGE IN PRODUCTION OF HYPOTONIC URINE (ADH ABSENT)280280028280H2OUrea10010028028010002803015%offiltr.28030%offiltr.280280NaClNaClH2OH2ONaClH2OH2O300100300NaCl300H2ONaClH2O325NaClH2O 150350H2ONaClH2ONaClH2O40040015% of filtrateNote: Figures given areexemplary rather than specific375H2ONaCl175375H2O350NaClH2O375375Urea75H2ONaClNaCl350375100325125325H2O350H2ONaCl350325NaClH2O300325Cortex15fil %tra ote f100280100% offiltrate280MedullaUreaH 2O280 lNa C280Na Cl NaClH2OUreaUreaNaCl040NaClH2O5040010%of filtr.Figure 18.3 Dilution of Urine Excess extracellular fluid (ECF) will decrease antidiuretic hormone (ADH)secretion and reduce water channels in the collecting ducts.
The disruption of the interstitial concentrationgradient and lack of water channels produce diuresis.determined by subtracting the osmolar clearance from theurine flow rate,..CH2O = V − (Uosm/Posm) × VThus, in dilute urine (e.g., U/P is less than 1) the CH2O isa positive number, implying that water was excreted. Incontrast, if the urine is concentrated (e.g., U/P is greater than1), the CH2O is negative, implying that water was retained.
Ifurine osmolarity equals plasma osmolarity, the CH2O equalszero.224Renal PhysiologyCLINICAL CORRELATEChronic PyelonephritisPyelonephritis is inflammation of the renal pelvis, caused by bacterial infection. While acute kidney infections are usually causedby urinary tract infections (UTI), they can recur, and with eachoccurrence they can further damage the kidney. UTIs typicallyarise from contamination from bowel microorganisms, althoughwith recurring infections that reach the kidney, potential underlying causes such as kidney stones or other anatomical abnormalities should be considered. Increased risk of pyelonephritis isassociated with diabetes, pregnancy, prostate enlargement, compromised immunity, and sexual behavior and spermicide use.The complications arising from chronic pyelonephritis relate tothe area that is infected. The smooth muscle lining of the renalpelvis exhibits peristaltic activity that helps direct the newly col-Possible routes of kidney infectionlected urine toward the ureters for transit to the urinary bladder.The infection causes abscesses and necrosis of the pelvic tissue,which can lead to fibrosis and scarring.As more of the medulla (tubules and parenchyma) becomesdamaged with repeated infections, the ability to maintain theinterstitial concentration gradient is compromised.
Because highinterstitial osmolarity provides the gradient that allows ADHdependent free water reabsorption and urine concentration, lossof the deep gradient restricts the ability to excrete concentratedurine and thus can cause polyuria, despite dietary water restriction. The loss of tubules also reduces glomerular filtration rate(GFR), and thus renal function as a whole is diminished.Pyelonephritis is treated with antibiotics over a period of severalweeks.
Increased fluid intake is recommended to flush any lowerurinary tract bacteria out though increased urine production.Predisposing factors in acute pyelonephritisAnomalies of kidney and/or ureterCalculiObstruction at any level (mechanical or functional)A. HematogenousB. Ascending(ureteral reflux)Diabetes mellitusPregnancyNeurogenic bladderInstrumentationAcute pyelonephritis.Radiating yellowish-gray streaks inpyramids and abscesses in cortex;moderate hydronephrosis withinfection; blunting of calyces(ascending infection)Acute pyelonephritis. With exudate chiefly of polymorphonuclearleukocytes in interstitium and collecting tubulesChronic pyelonephritis.Thinning of renal parenchyma.With wedge-shaped subcapsularscars; blurring of corticomedullaryjunction; dilated, fibrosed pelvisand calyces seen in many butnot all cases of chronicpyelonephritisChronic pyelonephritis.
Areas of lymphocytic infiltrationalternating with areas of relatively normal parenchymaChronic and Acute Pyelonephritis225CHAPTER19Regulation of Extracellular FluidVolume and OsmolarityHenle (TALH) and decreased water reabsorption in thethin descending limb of Henle (tDLH). The reductionin sodium reabsorption in the loop of Henle will increasethe delivery of sodium and fluid to the distal tubules andcollecting ducts (CDs). Because the concentration gradient is reduced, urine will not be effectively concentrated,and natriuresis/diuresis will occur.INTRARENAL REGULATION OF SODIUM ANDFLUID REABSORPTIONRenal sodium handling is closely regulated as part of theimportant process of extracellular fluid (ECF) homeostasis.
Anumber of intrarenal factors can alter sodium (and thus,fluid) reabsorption in response to changes in systemic volumestatus:■■■■Glomerular filtration rate (GFR): Increases in GFR willincrease the filtered load of sodium, and because the percentage of sodium reabsorbed in the proximal tubule doesnot change, the absolute amount of sodium entering theloop of Henle increases.
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