201. Consider the following statements about renal regulation.
I. Osmoreceptors respond to changes in body-fluid volume and ionic concentration.
II. The JGA responds when glomerular flow or GFR falls.
III. Increased atrial filling can stimulate ANF release.
IV. ADH, renin and ANF are all released in response to the same initiating signal.
ⓐ. I, II and III only
ⓑ. I and IV only
ⓒ. II, III and IV only
ⓓ. I, II, III and IV
Correct Answer: I, II and III only
Explanation: Kidney regulation involves several sensing systems with distinct initiating conditions. Osmoreceptors monitor changes related to body-fluid volume and ionic concentration and influence ADH release. The juxtaglomerular apparatus responds to reduced glomerular flow or GFR and can initiate renin release. Atrial tissue responds to increased filling by releasing ANF. Statements I, II and III are accurate, while statement IV incorrectly merges these different triggers. The regulators may all influence water, sodium, pressure or filtration, but they begin from different physiological disturbances and may produce opposing effects. Preserving these signal distinctions is essential for understanding feedback control rather than memorising hormones as interchangeable kidney regulators. Thus the first three statements preserve the distinct initiating signals, whereas the fourth incorrectly treats all three regulatory pathways as one response.
202. Prolonged sweating reduces body-water volume and raises the effective ionic concentration of body fluids. Glomerular function remains adequate. The most appropriate immediate regulatory sequence is:
ⓐ. atrial stretching \(\rightarrow\) ANF release \(\rightarrow\) reduced sodium-water retention
ⓑ. JGA suppression \(\rightarrow\) reduced renin \(\rightarrow\) increased sodium-water loss
ⓒ. osmoreceptor inhibition \(\rightarrow\) reduced ADH \(\rightarrow\) increased water reabsorption
ⓓ. osmoreceptor activation \(\rightarrow\) increased ADH \(\rightarrow\) increased water reabsorption
Correct Answer: osmoreceptor activation \(\rightarrow\) increased ADH \(\rightarrow\) increased water reabsorption
Explanation: Prolonged sweating removes body water and raises the effective ionic concentration of the remaining fluids. Osmoreceptors detect this change and stimulate a hypothalamically controlled response that increases ADH release from the neurohypophysis. ADH raises water permeability in later tubular regions and collecting ducts, allowing more water to be reabsorbed into the hyperosmotic renal medulla and returned to blood. Urine volume falls and the retained water helps restore fluid volume and osmolarity. Atrial stretching and ANF release are more typical of excessive blood volume, not dehydration. Suppressing the JGA or ADH would promote continued sodium-water loss and worsen the disturbance. Since glomerular function is stated to remain adequate, the immediate need is conservation of filtered water rather than repair of filtration. The causal sequence is therefore osmoreceptor activation, increased ADH and increased water reabsorption. The combined response conserves water through ADH while reduced perfusion can independently activate pressure-supporting renin release.
203. A graph has effective ADH action on the horizontal axis. Curve P, representing urine volume, falls as ADH action increases. Curve Q, representing urine concentration, rises over the same range. The graph is best interpreted as showing that ADH:
ⓐ. increases diuresis while reducing collecting-duct water recovery
ⓑ. increases water reabsorption, producing less but more concentrated urine
ⓒ. creates the medullary gradient without assistance from the loop of Henle
ⓓ. raises urine volume and concentration simultaneously through filtration
Correct Answer: increases water reabsorption, producing less but more concentrated urine
Explanation: Increasing ADH action makes late nephron regions and collecting ducts more effective at recovering water from tubular fluid. As more water returns toward the blood, less remains for excretion, producing the downward urine-volume curve P. Solutes retained in the remaining tubular fluid occupy a smaller water volume, so urine concentration rises along curve Q. These opposite trends express reduced diuresis rather than increased urine production. ADH uses the corticomedullary osmotic gradient but does not independently create the entire gradient, which depends on loop, vasa-recta and solute-recycling mechanisms. The graph demonstrates the functional outcome of ADH-controlled water conservation under otherwise comparable renal conditions. Greater ADH action increases collecting-duct water permeability, so more water returns to body fluids and less remains to dilute the final urine. The two curves are reciprocal consequences of one water-recovery mechanism.
204. After rapid intake of excess water, body-fluid volume rises and the osmotic stimulus to hypothalamic osmoreceptors falls. The expected response is:
ⓐ. reduced ADH release, reduced water recovery and increased dilute urine
ⓑ. increased ADH release, increased water recovery and increased dilute urine
ⓒ. increased renin release, increased water recovery and reduced atrial filling
ⓓ. reduced ANF release, increased sodium retention and reduced urine formation
Correct Answer: reduced ADH release, reduced water recovery and increased dilute urine
Explanation: Osmoreceptor signalling changes with body-fluid volume and ionic concentration. Following excess water intake, body fluids become relatively expanded and the stimulus that normally promotes ADH release is suppressed. Less ADH is released from the neurohypophysis under hypothalamic control, so late tubular regions and collecting ducts recover less water. A greater fraction of the filtered water remains in tubular fluid and is excreted as a larger volume of relatively dilute urine. This response helps remove the excess water and return body-fluid conditions toward their normal range. The pathway differs from renin release, which is associated mainly with reduced glomerular flow or pressure, and from ANF suppression, since increased atrial filling tends to favour ANF release.
205. Assertion: ADH may raise blood pressure through vasoconstriction.
Reason: ADH produces this vascular effect by relaxing vascular smooth muscle.
ⓐ. Both Assertion and Reason are true, and Reason correctly explains Assertion
ⓑ. Both Assertion and Reason are true, but Reason does not explain Assertion
ⓒ. Assertion is true, but Reason is false
ⓓ. Assertion is false, but Reason is true
Correct Answer: Assertion is true, but Reason is false
Explanation: ADH is also called vasopressin, reflecting its capacity to produce vascular constriction in addition to its antidiuretic action on the kidney. Constriction of blood vessels can increase vascular resistance and support a rise in blood pressure. Under suitable conditions, this may improve glomerular blood flow and help support GFR. The reason gives the opposite vascular mechanism. Relaxation of vascular smooth muscle produces vasodilation rather than vasoconstriction and would tend to lower vascular resistance. ADH’s water-conserving and vascular actions are related in their overall support of circulation during fluid loss, but they operate through different immediate effects: increased renal water recovery and constriction of blood vessels. Thus the assertion is true, but the reason is false: vascular smooth-muscle relaxation would produce vasodilation, whereas the pressure-raising vascular action described in the assertion requires constriction. ADH also promotes renal water reabsorption, but that separate action does not make the stated vascular reason correct.
206. An isolated vascular preparation constricts after ADH is added. In an intact renal preparation exposed to the same hormone, arterial pressure and a previously depressed GFR rise while the filtration barrier remains unchanged. The observations most strongly support the conclusion that ADH:
ⓐ. directly establishes the medullary gradient by producing urea
ⓑ. converts angiotensin I into angiotensin II in the circulation
ⓒ. increases filtration by opening pores for plasma proteins
ⓓ. supports filtration through pressure-raising vascular action
Correct Answer: supports filtration through pressure-raising vascular action
Explanation: The isolated preparation shows that ADH can narrow blood vessels, establishing a direct vascular effect. In the intact preparation, the rise in arterial pressure occurs together with recovery of GFR, while the filtration barrier remains structurally unchanged. This pattern supports a haemodynamic explanation: vasoconstriction raises pressure and can improve the pressure conditions supporting glomerular filtration. The observations do not show production of the medullary gradient, which depends mainly on loop, vasa recta and solute-recycling mechanisms. They also provide no evidence that ADH participates in the angiotensin-conversion sequence or makes the filtration barrier abnormally permeable. The experiment links ADH-induced vasoconstriction with support of renal blood pressure and filtration. Because barrier integrity is unchanged, recovery of GFR is attributed to pressure support rather than altered filtrate selectivity. Since barrier selectivity is unchanged, improved filtration is attributed to haemodynamic support rather than increased permeability of the filtration layers.
207. Two individuals show the following findings.
| Individual | Effective ADH action | Urine volume | Urine concentration | Glucose or ketones |
|---|
| P | Very low | High | Low | Absent |
| Q | Normal | Variable | Variable | Present |
The most appropriate classification is:
ⓐ. P-diabetes mellitus; Q-diabetes insipidus
ⓑ. P-diabetes insipidus; Q-diabetes mellitus
ⓒ. P-uremia; Q-diabetes insipidus
ⓓ. P-glomerulonephritis; Q-uremia
Correct Answer: P-diabetes insipidus; Q-diabetes mellitus
Explanation: Individual P has very low effective ADH action, excessive urine production and poorly concentrated urine. This combination is characteristic of diabetes insipidus at the elementary level: insufficient ADH action prevents adequate water recovery from late tubular regions and collecting ducts, increasing dehydration risk. The absence of glucose or ketones helps separate this condition from diabetes mellitus. Individual Q has normal ADH action but glucose or ketone bodies in urine, findings associated with diabetes mellitus in this context. The table must be interpreted through mechanism and composition together. A large urine volume alone is not enough to identify either disorder, and the word diabetes does not mean that both conditions share the same hormonal defect or urinary abnormality. ADH-related water loss and glucose-related metabolic findings must therefore be traced to different physiological pathways even when both conditions produce frequent urination.
208. A person has a normal corticomedullary osmotic gradient and normal glomerular filtration, but effective ADH action is severely deficient. A large volume of dilute urine is produced, and body-water loss increases. The primary defect is:
ⓐ. excessive sodium retention caused by persistent ANF release
ⓑ. failure to establish the filtration barrier around the glomerulus
ⓒ. excessive glucose filtration caused by aldosterone deficiency
ⓓ. failure to exploit the medullary gradient for water recovery
Correct Answer: failure to exploit the medullary gradient for water recovery
Explanation: The intact medullary gradient provides an osmotic force that could draw water from tubular fluid, but effective water movement also requires ADH-dependent permeability in late nephron regions and collecting ducts. Severe deficiency of ADH action prevents normal use of the existing gradient. More water remains in the tubular fluid, producing excessive dilute urine and increasing the risk of dehydration. Normal glomerular filtration and an intact gradient exclude a primary failure of filtrate formation or counter-current organisation. The case represents the basic ADH-related mechanism of diabetes insipidus. It also illustrates that creation of the medullary gradient and hormonal use of that gradient are separate requirements for production of concentrated urine. The defect lies in hormonal use of the gradient, so dilute urine persists despite normal filtration and intact counter-current architecture.
209. Assertion: Diabetes insipidus is defined by glucose appearing in urine due to deficient insulin action.
Reason: Deficient ADH action can cause excessive production of dilute urine without glycosuria being the defining feature.
ⓐ. Both Assertion and Reason are true, and Reason correctly explains Assertion
ⓑ. Both Assertion and Reason are true, but Reason does not explain Assertion
ⓒ. Assertion is true, but Reason is false
ⓓ. Assertion is false, but Reason is true
Correct Answer: Assertion is false, but Reason is true
Explanation: Diabetes insipidus is an ADH-related disorder in which deficient hormone action reduces renal water recovery. The resulting urinary pattern is excessive production of dilute urine, with increased danger of body-water depletion. Glucose in urine is not its defining feature. Glycosuria and ketonuria are instead associated with diabetes mellitus in the urinary findings covered here. The assertion incorrectly combines the name of one disorder with the mechanism and urinary sign of another. The reason correctly separates them by identifying the water-balance defect caused by inadequate ADH action. The shared word diabetes should not obscure the biological distinction between failure of antidiuretic regulation and abnormal glucose-related metabolism. The reason identifies the ADH-related water-balance defect and directly contradicts the false glucose-based definition in the assertion.
210. Consider the following statements about diabetes insipidus.
I. It may result from deficient ADH action.
II. It is associated with excessive loss of dilute urine.
III. It can increase the risk of dehydration.
IV. Glycosuria is its defining urinary abnormality.
ⓐ. I and IV only
ⓑ. II, III and IV only
ⓒ. I, II and III only
ⓓ. I, II, III and IV
Correct Answer: I, II and III only
Explanation: Deficient ADH action reduces water reabsorption from later tubular regions and collecting ducts. A greater volume of water remains in tubular fluid and leaves the body as dilute urine, supporting statements I and II. Continued excessive water loss can lower body-fluid volume and create a risk of dehydration, so statement III is also valid. Statement IV confuses diabetes insipidus with diabetes mellitus. Glucose in urine is associated with the latter disorder and is not the defining feature of inadequate ADH action. The valid set joins the hormonal defect, its renal consequence and the resulting homeostatic risk while excluding an unrelated diagnostic marker. Deficient ADH action, dilute polyuria and dehydration risk form one consistent set; glycosuria belongs to a different disorder.
211. Arrange the events of the renin-angiotensin pathway in their functional order.
P. Reduced GFR activates the juxtaglomerular apparatus.
Q. Renin is released into the blood.
R. Angiotensinogen is converted into angiotensin I.
S. Angiotensin I gives rise to angiotensin II.
T. Vasoconstriction and aldosterone-related responses are initiated.
ⓐ. \(Q \rightarrow P \rightarrow R \rightarrow T \rightarrow S\)
ⓑ. \(P \rightarrow Q \rightarrow R \rightarrow S \rightarrow T\)
ⓒ. \(P \rightarrow R \rightarrow Q \rightarrow S \rightarrow T\)
ⓓ. \(R \rightarrow P \rightarrow S \rightarrow Q \rightarrow T\)
Correct Answer: \(P \rightarrow Q \rightarrow R \rightarrow S \rightarrow T\)
Explanation: A fall in glomerular blood flow, pressure or GFR is detected at the juxtaglomerular apparatus. Juxtaglomerular cells respond by releasing renin into the circulation. Renin initiates the conversion of circulating angiotensinogen into angiotensin I, which is subsequently converted into angiotensin II. Angiotensin II is a strong vasoconstrictor and also stimulates aldosterone release from the adrenal cortex. These effects support blood pressure, sodium-water recovery and restoration of renal filtration conditions. The sequence must begin with the renal disturbance and its detection; the active pressure-raising responses appear only after formation of angiotensin II. Each stage supplies the condition required for the next stage in the pathway. Renin acts upstream of angiotensin formation, and angiotensin-II-related vascular and aldosterone effects occur downstream. This causal dependency excludes any order that places the pressure-supporting response before renin release. Each product becomes the condition for the next step, so angiotensin-II effects cannot precede renin action on angiotensinogen.
212. Use the pathway described below. Substance P is released from modified cells near the afferent arteriole after a fall in GFR. P acts on circulating substance Q to produce R, which is converted into vasoconstrictor S. Identify P, Q, R and S.
ⓐ. P-ADH, Q-angiotensinogen, R-angiotensin II, S-aldosterone
ⓑ. P-aldosterone, Q-renin substrate, R-renin, S-angiotensin I
ⓒ. P-renin, Q-angiotensinogen, R-angiotensin I, S-angiotensin II
ⓓ. P-ANF, Q-angiotensinogen, R-aldosterone, S-angiotensin II
Correct Answer: P-renin, Q-angiotensinogen, R-angiotensin I, S-angiotensin II
Explanation: Modified juxtaglomerular cells near the afferent arteriole release renin when glomerular flow, pressure or GFR falls. Renin acts on angiotensinogen circulating in blood and initiates formation of angiotensin I. Angiotensin I is then converted into angiotensin II, the potent vasoconstrictor named in the final clue. The identities are fixed by the release site, substrate-product order and vascular action. Aldosterone appears later after stimulation of the adrenal cortex, while ADH and ANF belong to regulatory pathways with different initiating signals. Reconstructing all four labels prevents the common errors of treating renin as the final vasoconstrictor or reversing angiotensin I and angiotensin II. Thus renin initiates the sequence, angiotensinogen is its circulating substrate, angiotensin I is the intermediate and angiotensin II is the vasoconstrictor product. Aldosterone is not one of the four labels because it acts later, after angiotensin II stimulates the adrenal cortex.
213. In an experiment, renal perfusion pressure is lowered while blood composition and tubular integrity remain unchanged. Renin concentration rises. When perfusion pressure is restored, renin release falls toward its initial level. The strongest inference is:
ⓐ. renin release rises when renal perfusion and filtration decline
ⓑ. renin is released mainly when atrial filling becomes excessive
ⓒ. renin directly makes collecting ducts impermeable to water
ⓓ. glomerular pressure rises only after ANF secretion increases
Correct Answer: renin release rises when renal perfusion and filtration decline
Explanation: The experiment changes renal perfusion pressure while preserving blood composition and tubular integrity, allowing the renin response to be linked to the vascular disturbance. Lower pressure is followed by increased renin, and restoration of pressure reduces the signal. This reversible pattern is consistent with activation of juxtaglomerular cells when glomerular blood flow, pressure or GFR falls. No atrial stretch or direct action of renin on collecting-duct water permeability is involved in the observed response. Renin initiates the angiotensin pathway rather than serving as the final effector at the tubule. The observations reveal a feedback response that is switched on by reduced renal filtration conditions and reduced when those conditions improve. The reversible rise and fall of renin with perfusion pressure demonstrates a feedback response to renal haemodynamic conditions rather than permanent secretion.
214. Formation of angiotensin II remains normal, and it continues to stimulate aldosterone release, but its vasoconstrictor action is selectively blocked. After a fall in GFR, the expected response is:
ⓐ. complete loss of sodium-water recovery and normal pressure restoration
ⓑ. increased vasoconstriction with reduced aldosterone secretion
ⓒ. complete restoration of GFR without any change in blood volume
ⓓ. preserved sodium-water retention but weakened rapid pressure support
Correct Answer: preserved sodium-water retention but weakened rapid pressure support
Explanation: Angiotensin II supports recovery through two linked branches. Its direct vasoconstrictor action raises vascular resistance and helps increase blood pressure and glomerular pressure. It also stimulates the adrenal cortex to release aldosterone, which promotes distal sodium and water reabsorption and gradually supports blood volume. The experimental block removes only the vascular branch, leaving aldosterone stimulation intact. Sodium-water retention can still occur, but the rapid pressure-raising effect produced by vasoconstriction is weakened. The pathway is not completely inactive, nor can normal restoration be assumed when one of its major effects is missing. The predicted pattern separates the immediate vascular contribution of angiotensin II from its indirect fluid-retaining contribution. Preservation of neighbouring renal processes localises the failed response to the renin-angiotensin-aldosterone pathway. Aldosterone-dependent sodium-water recovery can still occur, but loss of angiotensin-II vasoconstriction weakens the rapid pressure-supporting branch of the response.
215. Match each component with its appropriate role. Each Column II entry is used once.
| Column I | Column II |
|---|
| P. Juxtaglomerular apparatus | I. Increases distal \(\mathrm{Na^+}\) and water reabsorption |
| Q. Renin | II. Releases a signal after reduced GFR |
| R. Angiotensin II | III. Initiates conversion of angiotensinogen |
| S. Aldosterone | IV. Causes vasoconstriction and stimulates adrenal cortex |
ⓐ. \(\text{P-III, Q-II, R-I, S-IV}\)
ⓑ. \(\text{P-II, Q-III, R-IV, S-I}\)
ⓒ. \(\text{P-I, Q-IV, R-II, S-III}\)
ⓓ. \(\text{P-IV, Q-I, R-III, S-II}\)
Correct Answer: \(\text{P-II, Q-III, R-IV, S-I}\)
Explanation: The juxtaglomerular apparatus contains the modified cells that respond to reduced glomerular flow or GFR by releasing renin, so P maps to II. Renin initiates conversion of angiotensinogen, linking Q with III. Angiotensin II is the strong vasoconstrictor and also stimulates the adrenal cortex, so R maps to IV. Aldosterone acts on distal tubular regions to increase \(\mathrm{Na^+}\) and water reabsorption, placing S with I. The mapping follows the pathway from sensing and signal initiation to vascular and tubular effects. It also separates renin, an initiating signal, from angiotensin II and aldosterone, which produce different downstream responses. Renin, angiotensinogen, angiotensin II and aldosterone are distinguished by their positions and roles in the regulatory pathway.
216. Assertion: Angiotensin II stimulates the adrenal medulla to release aldosterone.
Reason: Aldosterone released from the adrenal cortex increases distal \(\mathrm{Na^+}\) and water reabsorption.
ⓐ. Both Assertion and Reason are true, and Reason correctly explains Assertion
ⓑ. Both Assertion and Reason are true, but Reason does not explain Assertion
ⓒ. Assertion is true, but Reason is false
ⓓ. Assertion is false, but Reason is true
Correct Answer: Assertion is false, but Reason is true
Explanation: Angiotensin II does stimulate aldosterone release, but the hormone comes from the adrenal cortex rather than the adrenal medulla. The assertion is false due to this incorrect anatomical source. The reason accurately describes both the source and the renal effect of aldosterone. By increasing sodium reabsorption in distal tubular regions, aldosterone promotes accompanying water recovery, helping raise blood volume and pressure. This response forms the fluid-retaining branch of the renin-angiotensin-aldosterone system. Correct understanding requires three linked distinctions: angiotensin II is the stimulating signal, the adrenal cortex releases aldosterone, and distal nephron transport provides the sodium-water response. Therefore, the aldosterone effect is described correctly, but its source is the adrenal cortex, not the medulla.
217. Four renal responses are recorded after separate hormonal treatments.
| Treatment | Distal \(\mathrm{Na^+}\) recovery | Water recovery | Blood-volume effect |
|---|
| P | Unchanged | Increased | Moderate rise |
| Q | Reduced | Reduced | Fall |
| R | Increased | Increased | Rise |
| S | Unchanged | Unchanged | No change |
Which treatment pattern is most consistent with increased aldosterone action?
ⓐ. P
ⓑ. Q
ⓒ. R
ⓓ. S
Correct Answer: R
Explanation: Aldosterone promotes sodium reabsorption in distal tubular regions. Water follows the retained sodium under appropriate physiological conditions, increasing recovery of both sodium and water and supporting a rise in blood volume. Treatment R shows this complete pattern. Treatment P resembles a primarily water-directed effect without the expected increase in distal sodium recovery. Treatment Q represents loss rather than enhancement of aldosterone-like action, while treatment S shows no effective response. The table must be interpreted across all three columns, since increased water recovery alone is not enough to identify aldosterone. The combined sodium, water and blood-volume changes distinguish the hormone’s fluid-retaining role within the renin-angiotensin-aldosterone pathway. Aldosterone favours distal sodium recovery; water retention follows the conserved solute and contributes to expansion of blood volume. The correct row must show all three changes in the same physiological direction.
218. Severe blood loss lowers renal perfusion and GFR. The juxtaglomerular apparatus remains functional, and the adrenal cortex responds normally. The coordinated response most likely to support restoration is:
ⓐ. renin, angiotensin-II vasoconstriction and aldosterone-driven sodium retention
ⓑ. ANF release, widespread vasodilation and reduced distal sodium recovery
ⓒ. reduced renin release, reduced vascular resistance and increased dilute urine
ⓓ. suppression of angiotensin II with reduced blood volume and pressure
Correct Answer: renin, angiotensin-II vasoconstriction and aldosterone-driven sodium retention
Explanation: Blood loss reduces circulating volume, renal perfusion and glomerular filtration. The juxtaglomerular apparatus responds by releasing renin, which initiates formation of angiotensin II. Angiotensin II constricts blood vessels, supporting blood pressure and glomerular pressure, and stimulates aldosterone release from the adrenal cortex. Aldosterone increases distal sodium and water reabsorption, helping rebuild blood volume. These vascular and tubular responses work together rather than acting as interchangeable steps. ANF is more closely associated with excessive atrial filling and would oppose fluid retention. The case requires integration of the initiating disturbance, renal sensor, circulating pathway and final pressure-volume effects that collectively support recovery of filtration.
219. Let \(G\) represent GFR, \(R\) renin release, \(AII\) angiotensin-II action and \(Ald\) aldosterone action. Which relation best represents the response to a fall in filtration?
ⓐ. \(G\downarrow \rightarrow R\downarrow \rightarrow AII\downarrow \rightarrow Ald\downarrow \rightarrow \text{pressure falls further}\)
ⓑ. \(G\downarrow \rightarrow R\uparrow \rightarrow AII\uparrow \rightarrow Ald\uparrow \rightarrow \text{pressure and volume are supported}\)
ⓒ. \(G\downarrow \rightarrow R\uparrow \rightarrow AII\downarrow \rightarrow Ald\downarrow \rightarrow \text{water loss decreases}\)
ⓓ. \(G\downarrow \rightarrow R\downarrow \rightarrow AII\uparrow \rightarrow Ald\uparrow \rightarrow \text{vasodilation increases}\)
Correct Answer: \(G\downarrow \rightarrow R\uparrow \rightarrow AII\uparrow \rightarrow Ald\uparrow \rightarrow \text{pressure and volume are supported}\)
Explanation: A fall in GFR is detected by the juxtaglomerular apparatus and stimulates renin release, represented by \(G\downarrow\rightarrow R\uparrow\). Renin initiates formation of angiotensin II, so \(AII\uparrow\) follows. Angiotensin II causes vasoconstriction and stimulates the adrenal cortex to release aldosterone, giving \(Ald\uparrow\). Aldosterone increases sodium reabsorption in distal nephron regions, and water follows the retained solute. Together with vasoconstriction, this supports circulating volume, arterial pressure and the pressure conditions needed for glomerular filtration. The complete relation is \(G\downarrow\rightarrow R\uparrow\rightarrow AII\uparrow\rightarrow Ald\uparrow\), followed by support of pressure and volume. Every arrow must preserve the feedback direction. Initial low filtration does not normally suppress renin, angiotensin II is not a vasodilator, and aldosterone does not promote sodium-water loss. The symbolic chain links detection, hormonal sequence and compensatory outcome in one regulated pathway.
220. Isolated atrial tissue is stretched to imitate increased filling. ANF release rises, and fluid containing the released factor causes relaxation of a vascular preparation. The strongest conclusion is:
ⓐ. atrial stretch can trigger a pressure-lowering vasodilator signal
ⓑ. atrial stretch directly activates juxtaglomerular renin secretion
ⓒ. ANF produces its effect by increasing angiotensin-II formation
ⓓ. ANF is released mainly when body-fluid volume becomes deficient
Correct Answer: atrial stretch can trigger a pressure-lowering vasodilator signal
Explanation: The treatment imitates increased blood return and atrial filling by physically stretching atrial tissue. The first observation links this mechanical stimulus with increased ANF release. Fluid containing the released factor then relaxes the vascular preparation, establishing a vasodilator action rather than merely an association with atrial tissue. Vasodilation lowers vascular resistance and supports reduction of excessive blood pressure. In the intact body, ANF also opposes the renin-angiotensin-aldosterone pathway and favours loss of sodium and water, reinforcing the same volume-lowering direction. The observations do not demonstrate renin activation or increased angiotensin-II formation; those belong to a pressure-raising pathway associated with reduced renal perfusion. ANF is released in response to excessive filling rather than volume deficiency. The strongest inference therefore links atrial stretch to a pressure-lowering vasodilator signal while staying within the evidence supplied by the preparation.
