Kidney Function & Electrolyte Balance

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Questions and Answers

Match the diuretic with its primary site of action within the nephron and its effect on calcium excretion:

Furosemide = Thick ascending limb; increases urinary calcium excretion Thiazides = Distal convoluted tubule; reduces urinary calcium excretion Amiloride = Collecting duct; potassium-sparing, minimal effect on calcium Acetazolamide = Proximal tubule; primarily affects bicarbonate reabsorption, indirect effect on calcium

Associate the cell type found in the late distal tubule and collecting duct with its primary function in electrolyte balance:

Principal cells = Sodium reabsorption and potassium secretion, regulated by aldosterone Intercalated cells = Acid-base balance through hydrogen ion secretion or bicarbonate secretion Juxtaglomerular cells = Renin secretion in response to decreased renal perfusion pressure Mesangial cells = Regulation of glomerular filtration rate via contraction and relaxation influenced by vasoactive substances

Correlate the functional characteristic of the thick ascending limb with its contribution to the formation of dilute or concentrated urine:

Impermeability to water = Generation of hypotonic tubular fluid due to solute reabsorption without water reabsorption Active reabsorption of Na+, Cl-, and K+ = Reduction of tubular fluid osmolality, contributing to dilute urine formation Paracellular reabsorption of Mg++ and Ca++ = Facilitation of divalent cation reabsorption driven by the electrochemical gradient Location of the macula densa = Regulation of glomerular filtration rate via tubuloglomerular feedback

Match the component of the juxtaglomerular apparatus with its specific role in regulating blood pressure and electrolyte balance:

Macula densa = Senses changes in NaCl concentration in the distal tubule and signals the JG cells Juxtaglomerular cells = Synthesizes and secretes renin in response to decreased blood pressure or sympathetic stimulation Extraglomerular mesangial cells = Provide structural support and mediate signals between macula densa and JG cells Afferent arteriole = Delivers blood to the glomerulus and is the primary site of renin secretion Signup and view all the answers

Relate the diuretic mechanism of action to the specific transporter inhibited and the resulting electrolyte disturbance:

Loop diuretics = Inhibition of Na-K-2Cl cotransporter; hypokalemia, hypomagnesemia, hypocalcemia Thiazide diuretics = Inhibition of Na-Cl cotransporter; hypokalemia, hypercalcemia Potassium-sparing diuretics = Inhibition of ENaC or aldosterone receptor antagonism; hyperkalemia Carbonic anhydrase inhibitors = Inhibition of carbonic anhydrase; hyperchloremic metabolic acidosis Signup and view all the answers

Match the specific segment of the nephron with its unique permeability characteristics and their physiological consequences:

Thick ascending limb = Impermeable to water; allows generation of dilute tubular fluid Proximal convoluted tubule = Highly permeable to water and solutes; facilitates isosmotic reabsorption Thin descending limb = Highly permeable to water, relatively impermeable to solutes; allows water reabsorption into the medullary interstitium Collecting duct = Variable permeability to water controlled by ADH; fine-tunes final urine osmolality Signup and view all the answers

Associate the mechanism of calcium reabsorption in the thick ascending limb with its underlying driving force:

Paracellular pathway = Driven by the electrochemical gradient created by back leak of potassium Transcellular pathway via TRPV5 channels = Primarily occurs in the distal convoluted tubule, not the thick ascending limb Active transport via Ca2+-ATPase = Plays a minor role compared to paracellular reabsorption in the thick ascending limb Sodium-calcium exchanger = Predominantly involved in calcium efflux rather than reabsorption Signup and view all the answers

Identify the key characteristic that distinguishes the 'early' distal tubule from the 'late' distal tubule and collecting duct:

Na-Cl cotransporter = Predominantly expressed in the early distal tubule; site of action for thiazide diuretics Aldosterone responsiveness = Characteristic of the late distal tubule and collecting duct; regulates sodium reabsorption Water permeability = Low in the early distal tubule, variable in the late distal tubule and collecting duct (ADH-dependent) Urea permeability = Low in both the early and late distal tubule. Signup and view all the answers

Match the following transport mechanisms in the nephron with their most accurate description under conditions of antidiuresis:

Aquaporin-2 Insertion = ADH-mediated increase in water permeability in the collecting duct. Urea Transporter UT-A1 = Facilitates urea reabsorption from the medullary collecting duct into the medullary interstitium, contributing to the corticomedullary osmotic gradient. Na-K-2Cl Symporter (NKCC2) = Active transport of these ions in the thick ascending limb of the loop of Henle, critical for establishing medullary hypertonicity. Vasa Recta Countercurrent Exchange = Minimizes solute washout from the renal medulla, maintaining the osmotic gradient necessary for water reabsorption. Signup and view all the answers

Match the following renal parameters with their expected changes in a patient with advanced chronic kidney disease (CKD) and significantly reduced GFR:

Plasma Urea Concentration = Significantly elevated due to decreased filtration and excretion. Fractional Excretion of Urea = May increase as a compensatory mechanism, but overall excretion is still reduced. Urine Output = Variable; may be decreased (oliguria) or increased (polyuria) depending on the stage and underlying cause of CKD. GFR = Substantially reduced, reflecting impaired kidney function. Signup and view all the answers

Match the following compounds with their primary mechanism of renal excretion or handling:

Urea = Filtered by the glomerulus and variably reabsorbed, primarily in the collecting duct and loop of Henle, influenced by ADH levels. Creatinine = Freely filtered and minimally secreted or reabsorbed, making it a reliable marker of GFR. Uric Acid = Complex handling involving filtration, reabsorption, and secretion; dysregulation can lead to hyperuricemia and gout. Glucose (in a healthy individual) = Freely filtered and completely reabsorbed in the proximal tubule by sodium-glucose cotransporters (SGLTs). Signup and view all the answers

In a scenario characterized by sustained hypovolemia leading to chronic activation of the renin-angiotensin-aldosterone system (RAAS), match the expected effects on the following nephron segments:

Proximal Tubule = Increased sodium and water reabsorption stimulated by angiotensin II, enhancing volume restoration at the expense of potentially exacerbating metabolic alkalosis. Loop of Henle = Enhanced sodium chloride reabsorption in the thick ascending limb, contributing to medullary hypertonicity and water conservation; however, prolonged activation can lead to tubulointerstitial fibrosis. Distal Tubule and Collecting Duct = Aldosterone-mediated increase in sodium reabsorption and potassium secretion, exacerbating potassium depletion and further contributing to metabolic alkalosis but crucial for maintaining blood pressure. Glomerulus = Angiotensin II-mediated vasoconstriction of the efferent arteriole to maintain GFR, but chronic vasoconstriction can lead to glomerular damage and eventual reduction in GFR. Signup and view all the answers

Match these classes of diuretics with their primary site of action within the nephron:

Loop Diuretics (e.g., Furosemide) = Inhibit the Na-K-2Cl symporter in the thick ascending limb of the loop of Henle, impairing medullary hypertonicity. Thiazide Diuretics (e.g., Hydrochlorothiazide) = Inhibit the Na-Cl symporter in the distal convoluted tubule, reducing sodium reabsorption. Potassium-Sparing Diuretics (e.g., Spironolactone) = Block aldosterone receptors in the collecting duct, decreasing sodium reabsorption and potassium secretion. Carbonic Anhydrase Inhibitors (e.g., Acetazolamide) = Inhibit carbonic anhydrase in the proximal tubule, reducing bicarbonate reabsorption. Signup and view all the answers

Match the nephron segment with its characteristic permeability to urea:

Proximal Tubule = Reabsorbs approximately 40% of filtered urea, but concentration increases due to higher water reabsorption. Thin Loop of Henle = Moderately permeable, allows urea to enter the lumen from the interstitium due to high interstitial concentration. Thick Ascending Limb = Impermeable to urea, leading to increased urea concentration in the tubular fluid. Medullary Collecting Duct = Slightly permeable to urea; permeability is enhanced by ADH. Signup and view all the answers

Match the following physiological conditions with their expected impact on the renal handling of glucose:

Normal GFR, Plasma Glucose = 150 mg/dL = Complete reabsorption of filtered glucose; no glucosuria. Normal GFR, Plasma Glucose = 300 mg/dL = Glucosuria present; glucose excretion rate is proportional to the amount exceeding $T_m$. Reduced GFR, Plasma Glucose = 300 mg/dL = Reduced glucosuria compared to normal GFR at the same plasma glucose due to decreased filtered load. SGLT2 Inhibitor Administration = Glucosuria even at normal plasma glucose levels due to reduced reabsorption in the proximal tubule. Signup and view all the answers

Given varying degrees of ADH influence, match the collecting duct segment with its resulting urea permeability:

Cortical Collecting Duct, Low ADH = Minimal urea permeability, contributing to lower urine concentration. Medullary Collecting Duct, Low ADH = Low urea permeability, limiting urea reabsorption into the medullary interstitium. Cortical Collecting Duct, High ADH = Remains relatively impermeable to urea despite ADH influence. Medullary Collecting Duct, High ADH = Increased urea permeability, enhancing urea recycling and the medullary osmotic gradient. Signup and view all the answers

Match each statement with its implications regarding the renal threshold and $T_m$ for glucose:

Renal threshold < $T_m$ = Splay phenomenon occurs; glucose excretion begins before all nephrons are saturated. Variable Nephron $T_m$ = Some nephrons excrete glucose at lower plasma concentrations than others. Renal threshold reached = Glucosuria is present, indicating the filtered load exceeds the reabsorptive capacity. Plasma Glucose < Renal Threshold = No glucosuria; filtered glucose is completely reabsorbed under normal conditions. Signup and view all the answers

Relate each condition to its associated impact on the tubular maximum ($T_m$) for glucose reabsorption:

Uncontrolled Diabetes Mellitus = Increased filtered glucose load, potentially exceeding the $T_m$. Advanced Renal Disease = Decreased $T_m$ due to reduced functional nephron mass. SGLT2 Inhibitor Therapy = Pharmacologically reduced $T_m$ by inhibiting glucose reabsorption. Normal Physiological Conditions = $T_m$ near the typical value of approximately 375 mg/min in healthy adults. Signup and view all the answers

Match the mechanism of action of each diuretic with its potential impact on urea handling in the nephron:

Loop Diuretics = Diminished medullary osmotic gradient due to reduced NaCl reabsorption, decreasing urea concentration in the medulla. Thiazide Diuretics = Increased distal delivery of fluid may enhance urea excretion, although less significant impact on medullary gradient compared to loop diuretics. Potassium-Sparing Diuretics = Minimal direct impact on urea handling; primarily affects sodium and potassium balance in the collecting duct. Osmotic Diuretics = Increased urine flow rate reduces the time available for urea reabsorption, leading to increased urea excretion. Signup and view all the answers

Match the specific clinical scenario with the expected alteration in glucose reabsorption dynamics:

Pregnancy-Induced Hyperfiltration = Increased GFR leads to a higher filtered glucose load, potentially causing glucosuria despite normal plasma glucose. Fanconi Syndrome = Impaired proximal tubular function results in glucosuria, aminoaciduria, and phosphaturia due to defective reabsorption. Renal Artery Stenosis = Reduced GFR in the affected kidney may decrease the filtered glucose load and reduce glucosuria compared to the contralateral kidney. Diabetic Nephropathy = Progressive damage to nephrons impairs both filtration and reabsorption, leading to variable glucosuria depending on the stage. Signup and view all the answers

Match the following physiological states with their expected impact on urea handling within the renal medulla:

High protein diet = Increased urea production enhances the medullary osmotic gradient. Water diuresis = Reduced medullary urea concentration results in a blunted osmotic gradient. Low protein diet = Impaired urine concentrating ability due to decreased urea levels. Infant (<1 year of age) = Reduced urine-concentrating ability due to protein utilization for growth and lower urea production. Signup and view all the answers

Match the specific type of urea transporter isoform with its primary location and regulatory mechanism within the kidney:

UT-A1 = Medullary collecting duct; upregulated by vasopressin (ADH) to enhance urea reabsorption and concentrate urine. UT-A2 = Descending vasa recta; facilitates urea entry into the medullary interstitium. UT-B = Erythrocytes and vasa recta; involved in systemic urea transport and potentially contributes to medullary urea handling. UT-A3 = Less understood function, may play a minor role in urea transport in specific nephron segments. Signup and view all the answers

Match the following components of the renal medulla with their specific osmoregulatory functions:

Descending limb of the loop of Henle = Water is drawn out, concentrating NaCl. Thin ascending limb of the loop of Henle = NaCl passively diffuses out into the interstitium. Vasa recta = Countercurrent exchange minimizes solute washout from the medulla. Medullary interstitium = High osmotic activity due to urea and NaCl. Signup and view all the answers

Match the following alterations in medullary blood flow with their predicted impact on the renal concentrating mechanism:

Increased medullary blood flow = Reduces the osmotic gradient by washing out solutes; impairs urine concentration. Decreased medullary blood flow = Maintains the osmotic gradient by minimizing solute washout; enhances urine concentration (up to physiological limit). Disruption of vasa recta countercurrent exchange = Reduces the osmotic gradient by impairing solute trapping; impairs urine concentration. Pharmacological vasodilation of medullary vasculature = Reduces medullary osmolality by increasing solute washout; impairs maximal urine concentrating ability. Signup and view all the answers

Match the following dietary conditions with their predicted effects on fractional urea excretion ($FE_{Urea}$), assuming normal renal function:

High protein diet = Decreased $FE_{Urea}$ due to increased urea reabsorption for medullary gradient maintenance. Low protein diet = Increased $FE_{Urea}$ due to reduced urea reabsorption as medullary gradient contribution is less critical. Normal protein diet = Baseline $FE_{Urea}$ reflecting balanced urea handling for osmotic gradient and excretion. Severe malnutrition = Markedly increased $FE_{Urea}$ due to significantly decreased urea production and negligible contribution to medullary gradient. Signup and view all the answers

Match the following experimental manipulations with their predicted impact on the maximum achievable urine osmolality in a rodent model:

Administration of vasopressin receptor antagonist = Significantly decreased urine osmolality due to impaired water reabsorption in collecting ducts. Genetic knockout of urea transporters in inner medullary collecting ducts = Moderately decreased urine osmolality due to reduced urea recycling and medullary gradient. Selective ablation of vasa recta capillaries = Severely decreased urine osmolality due to disruption of medullary osmotic architecture. Chronic administration of a loop diuretic = Moderately decreased urine osmolality due to reduced NaCl reabsorption in the ascending limb and impaired medullary gradient. Signup and view all the answers

Match the following pathological conditions with their expected effect on the urea concentration gradient within the renal medulla:

Chronic Kidney Disease (CKD) = Reduced urea production and impaired tubular function lead to a blunted medullary gradient. Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) = Increased water reabsorption dilutes the medullary interstitium, decreasing the urea concentration. Diabetes Insipidus (DI) = Insufficient ADH leads to reduced water reabsorption, impairing the formation of a concentrated medullary gradient. Hepatic Cirrhosis = Reduced urea production due to impaired hepatic function diminishes the medullary urea concentration. Signup and view all the answers

Match the following nephron segments with their relative urea permeability characteristics under conditions of maximal antidiuresis:

Proximal Tubule = Moderate permeability due to solvent drag. Descending Limb of Loop of Henle = Low permeability contributing to urea concentration. Ascending Limb of Loop of Henle = Very low permeability preventing urea reabsorption in this segment. Inner Medullary Collecting Duct = High permeability regulated by UT-A1 transporters facilitating urea recycling. Signup and view all the answers

Match the following therapeutic interventions with their primary mechanism of altering urea handling in the kidney:

Loop diuretics (e.g., Furosemide) = Inhibits Na-K-2Cl cotransporter in ascending limb, reducing medullary NaCl gradient and secondarily affecting urea recycling. Vasopressin analogs (e.g., Desmopressin) = Increases water permeability in collecting ducts, enhancing water reabsorption and indirectly concentrating urea in the medulla Lithium = Induces nephrogenic diabetes insipidus, impairing water reabsorption and disrupting the urea concentration gradient. Urea supplementation = Increases plasma urea concentration, enhancing urea delivery to the medulla and potentially improving concentrating ability (within limits). Signup and view all the answers

Match the following physiological factors with their corresponding effects on Glomerular Filtration Rate (GFR) under conditions mimicking severe hypovolemic shock, assuming complete failure of autoregulatory mechanisms:

Increased Sympathetic Nerve Activity (renal) = Profound reduction in GFR due to intense afferent arteriolar vasoconstriction mediated by norepinephrine and angiotensin II. Elevated Plasma Colloid Osmotic Pressure = Significant decrease in GFR as enhanced oncotic pressure in glomerular capillaries opposes filtration pressure. Marked Increase in Arterial Pressure (MAP > 150 mmHg) = Initially elevated GFR, quickly followed by a decrease due to glomerular capillary damage and back leak of filtrate. Presence of High Concentrations of Non-Reabsorbable Osmolytes (Mannitol) = Initially, a modest increase in GFR followed by a substantial decrease due to tubuloglomerular feedback activation and volume depletion. Signup and view all the answers

Match the following intrarenal hormonal and neural mechanisms with their specific effects on tubular sodium reabsorption during instances of escalating hemorrhage, assuming that compensatory responses are actively blunting deviations from normal blood pressure:

Increased Angiotensin II Production (ATII) = Significant enhancement of sodium and water reabsorption in proximal tubule, driven by increased Na+/H+ exchange activity. Elevated Plasma Aldosterone Levels = Augmented sodium reabsorption in the cortical collecting duct, coupled with increased potassium secretion, mediated by mineralocorticoid receptor activation. Increased Release of Atrial Natriuretic Peptide (ANP) = Minimal effect on sodium reabsorption due to counter-regulation by the sympathetic nerves system and elevated angiotensin II, which antagonize ANP's effects and limit natriuresis. Direct Sympathetic Nerve Stimulation of Renal Tubules = Augmentation of sodium reabsorption in multiple renal segments via α1-adrenergic receptor-mediated stimulation of Na+/K+-ATPase and increased expression of sodium transporters. Signup and view all the answers

Match the following scenarios of altered renal hemodynamics with their predicted steady-state effects on overall sodium excretion (UNaV), assuming a normally functioning nephron in a patient with chronic hypertension:

Selective Efferent Arteriolar Vasodilation (induced pharmacologically) = Significant reduction in UNaV due to lowered peritubular capillary hydrostatic pressure, promoting increased proximal tubular sodium reabsorption and enhanced ATII signaling. Combined Afferent and Efferent Arteriolar Vasoconstriction (equal magnitude) = Marginal change in UNaV as opposing effects on GFR and peritubular hydrostatic pressure largely cancel each other out and sodium handling shifts between segments. Increased Renal Interstitial Hydrostatic Pressure (due to urinary obstruction) = Significant elevation in UNaV due to impeded sodium reabsorption across the tubular epithelium and direct pressure effects on the peritubular capillaries. Pharmacologically Induced Blockade of Proximal Tubular Na+/H+ Exchangers (NHE3) = Marked increase in UNaV due to reduced proximal tubule sodium reabsorption. This effect will exhibit only transient changes with compensatory mechanisms. Signup and view all the answers

Match the following clinical interventions during septic shock with their expected effects on urine output, taking into account the complex interplay of hemodynamic and inflammatory factors:

Administration of High-Dose Vasopressors (norepinephrine) = Variable effect on urine output, initially decreasing due to increased afferent arteriolar vasoconstriction, however potential improvement perfusion could increase the urine output later. Aggressive Infusion of Crystalloid Fluids (normal saline) = Initially increased urine output due to increased GFR from increased plasma volume, however may result in anasarca if microvascular permeability is significantly increased. Therapeutic Implementation of Renal Replacement Therapy (RRT) = Controlled and predictable urine output, independent of intrinsic renal function, allowing for precise fluid balance management and solute clearance. Administration of Loop Diuretics (furosemide) to a Patient with Pre-existing Acute Tubular Necrosis = Minimal or no increase in urine output due to impaired diuretic response in damaged tubules, potentially exacerbating electrolyte imbalances. Signup and view all the answers

Match the following pathological states with their expected effects on the fractional excretion of urea (FEUrea), assuming normal renal perfusion pressure and glomerular filtration rate:

Severe Dehydration = Reduced FEUrea due to increased urea reabsorption driven by augmented sodium and water reabsorption in the proximal tubule; heightened urea recycling enhances medullary gradient. High-Protein Diet = Increased FEUrea due to elevated urea production and filtered load, surpassing the capacity for maximal urea reabsorption. Acute Tubular Necrosis (ATN) = Markedly increased FEUrea due to impaired tubular reabsorption of urea in injured segments, disrupting the corticomedullary gradient. Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) = Normal to slightly elevated FEUrea reflecting the increase in urine output and normal urea reabsorption, with a higher urine flow rate. Signup and view all the answers

Match the following pharmaceutical agents with their primary mechanisms of action affecting lithium clearance, assuming steady-state lithium levels in a patient with bipolar disorder and otherwise normal renal function:

Thiazide Diuretics (hydrochlorothiazide) = Significant reduction in lithium clearance due to enhanced proximal tubular reabsorption of sodium and lithium. Nonsteroidal Anti-Inflammatory Drugs (NSAIDs; ibuprofen) = Moderate decrease in lithium clearance due to prostaglandin inhibition, leading to decreased GFR and increased proximal tubular reabsorption. Angiotensin-Converting Enzyme Inhibitors (ACEIs; lisinopril) = Modest reduction in lithium clearance due to efferent arteriolar vasodilation and decreased GFR, though less pronounced effect than thiazides. Loop Diuretics (furosemide) = Transient and potentially variable effect on lithium clearance depending on hydration status; in dehydration it would further enhance lithium levels and concentration. Signup and view all the answers

Match the following experimental manipulations of collecting duct physiology with their anticipated effects on the urine osmolality in a rat model of diabetes insipidus (central type), assuming stable plasma osmolality:

Selective Knockout of Aquaporin-2 (AQP2) Channels = No effect on maximum achievable urine osmolality, as the constitutive water permeability is already compromised in diabetes insipidus. It depends on the severity of mutation. Administration of a V2 Receptor Agonist (desmopressin) = Significant increase in urine osmolality due to activation of V2 receptors, leading to increased cAMP production and insertion of AQP2 channels into the apical membrane of collecting duct cells. Blockade of Urea Transporters (UT-A1) in the Inner Medullary Collecting Duct = Substantial reduction in maximum urine osmolality due to impaired urea recycling, disrupting the medullary osmotic gradient necessary for maximal water reabsorption. Inhibition of Na+/K+-ATPase in Collecting Duct Principal Cells = Potentially reduce or no impact on urine osmolality, primarily due to decreased sodium reabsorption that diminishes water reabsorption via reduced osmotic gradient. Signup and view all the answers

Match each of the following scenarios of renal physiology to the most likely effect on the excretion of phosphate (PO4) by the kidney:

Treatment with a Fibroblast Growth Factor 23 (FGF23) Inhibitor = Significant increase in proximal tubule phosphate reabsorption causing decreased phosphate excretion with FGF23 inhibition. The effects are related to the suppression of sodium-dependent phosphate cotransporters and increased Vitamin D. Acute Respiratory Alkalosis = Increase in intracellular pH causes increased activity of the NaPi-IIa cotransporter increasing phosphate reabsorption in the proximal tubule. This leads to decreased PO4 excretion. Administration of Parathyroid Hormone (PTH) = Increase in phosphate excretion. PTH inhibits the NaPi-IIa cotransporter in the proximal tubule which reduces resorption. Volume Expansion (hypervolemia) = Increased phosphate excretion. Volume expansion inhibits proximal tubular sodium and phosphate reabsorption via natriuretic peptides and other volume-sensing mechanisms. Signup and view all the answers

Match the following effects of Angiotensin II on renal function with their corresponding mechanisms, assuming a scenario of moderate Angiotensin II concentration:

Increased Na+ and water reabsorption = Direct stimulation of Na+-K+ ATPase pump and Na+-H+ exchange in tubular cells. Increased colloid osmotic pressure in peritubular capillaries = Disproportionate filtration of plasma fluid leading to high protein concentration in efferent arteriolar blood. Reduced peritubular capillary pressure = Preferential constriction of efferent arterioles increasing resistance to outflow. GFR maintained near normal = Efferent arteriolar constriction offsetting afferent arteriolar constriction. Signup and view all the answers

Match the following mediators with their counter-regulatory actions against Angiotensin II in the renal vasculature:

Nitric Oxide (NO) = Vasodilation of afferent and efferent arterioles, counteracting Angiotensin II-induced vasoconstriction. Prostaglandins (PGE2, PGI2) = Attenuation of Angiotensin II's vasoconstrictive effects, particularly in the afferent arteriole, preserving RBF. Atrial Natriuretic Peptide (ANP) = Inhibition of renin secretion, reduction of Angiotensin II formation and vasodilation. Bradykinin = Stimulation of NO release, leading to vasodilation and antagonism of Angiotensin II's pressor effects. Signup and view all the answers

Match the following scenarios related to Angiotensin II and renal function with their expected net effect on Glomerular Filtration Rate (GFR):

Administration of a selective Angiotensin II type 1 (AT1) receptor blocker in a patient with heart failure = Increase in GFR due to reduced efferent arteriolar tone. Chronic Nonsteroidal Anti-Inflammatory Drug (NSAID) use in a patient with pre-existing renal artery stenosis = Significant decrease in GFR due to unopposed Angiotensin II-mediated vasoconstriction. Acute volume depletion with compensatory Angiotensin II activation = Relatively maintained GFR due to efferent arteriolar constriction counteracting hypoperfusion. Selective mesangial cell Angiotensin II receptor activation = Decrease in GFR due to reduced capillary filtration coefficient (Kf). Signup and view all the answers

Match the following conditions with their influence on the sensitivity of the renal arterioles to Angiotensin II:

Chronic hyperglycemia in diabetes mellitus = Increased sensitivity due to enhanced oxidative stress and impaired NO bioavailability. Pregnancy = Decreased sensitivity due to increased levels of vasodilatory factors. Aging = Increased sensitivity due to endothelial dysfunction and reduced renal reserve. Salt-sensitive hypertension = Increased sensitivity due to complex interactions involving the renin-angiotensin-aldosterone system. Signup and view all the answers

Match the following cellular mechanisms with their role in Angiotensin II-mediated regulation of tubular sodium reabsorption:

Activation of Na+/H+ exchanger isoform 3 (NHE3) in the proximal tubule = Increased apical sodium entry, leading to enhanced sodium and bicarbonate reabsorption. Phosphorylation and increased activity of the basolateral Na+-K+ ATPase = Enhanced sodium extrusion from the tubular cell, contributing to overall sodium reabsorption. Increased expression of the thiazide-sensitive Na+-Cl− cotransporter (NCC) in the distal convoluted tubule = Augmented sodium and chloride reabsorption in the distal nephron segment. Upregulation of epithelial sodium channel (ENaC) subunits in the collecting duct = Increased sodium reabsorption in the principal cells, regulated by aldosterone and Angiotensin II. Signup and view all the answers

Match the following scenarios of altered renal hemodynamics with the expected impact on Angiotensin II's influence on sodium reabsorption. Assume Angiotensin II levels are held constant:

Increased renal perfusion pressure = Attenuation of Angiotensin II-mediated sodium reabsorption due to pressure natriuresis. Decreased renal perfusion pressure = Potentiation of Angiotensin II-mediated sodium reabsorption as a compensatory mechanism. Selective afferent arteriolar vasodilation = Attenuation of Angiotensin II's effects on sodium reabsorption due to increased downstream hydrostatic pressure. Administration of a nitric oxide synthase (NOS) inhibitor = Potentiation of Angiotensin II's pro-reabsorptive effects due to reduced counter-regulatory vasodilation. Signup and view all the answers

Match the specific Angiotensin II-mediated signaling pathways with their respective downstream effectors in renal tubular cells:

Activation of phospholipase C (PLC) = Increased intracellular calcium levels, activation of protein kinase C (PKC), and modulation of transporter activity. Stimulation of mitogen-activated protein kinase (MAPK) pathways = Regulation of gene transcription, cellular growth, and differentiation. Activation of Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathways = Regulation of cytokine expression and inflammatory responses in renal cells. G-protein coupled receptor (GPCR) internalization and β-arrestin recruitment = Receptor desensitization and initiation of alternative signaling cascades. Signup and view all the answers

Match the following pathophysiological states with their characteristic alterations in the renal Angiotensin II system:

Hepatorenal Syndrome = Exaggerated intrarenal Angiotensin II activity contributing to renal vasoconstriction and sodium retention. Bartter Syndrome = Increased renin and Angiotensin II levels due to impaired sodium chloride reabsorption in the loop of Henle. Autosomal Dominant Polycystic Kidney Disease (ADPKD) = Upregulation of the intrarenal renin-angiotensin system promoting cyst growth and disease progression. Preeclampsia = Increased sensitivity to Angiotensin II contributing to hypertension and renal dysfunction. Signup and view all the answers

Flashcards

Loop Diuretics

Drugs like frusemide that inhibit the Na-K-2Cl co-transporter in the loop of Henle.

Macula Densa

Specialized cells in the thick ascending limb that monitor tubular fluid composition.

Juxtaglomerular (JG) Cells

Specialized smooth muscle cells in the afferent arteriole that store and release renin.

Juxtaglomerular Complex/Apparatus

The combination of macula densa, JG cells, and other cells that regulates blood pressure and filtration rate.