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Quizzes > Health & Medicine > Human Anatomy & Medicine

Think You Can Master the Endocrine System? Try the ADH Transport Quiz!

Ready to test your gland functions and hormone transport mechanism in this endocrine system quiz?

Difficulty: Moderate
2-5mins
Learning OutcomesCheat Sheet
Paper art glands hormones and ADH molecules traveling through bloodstream and vessels on a sky blue background

Are you ready to discover exactly how ADH travels to its target cells via the bloodstream? This engaging endocrine system quiz is designed for students, healthcare professionals, and curious minds eager to test their hormone function quiz knowledge and deepen their grasp of gland functions test. You'll explore the hormone transport mechanism that shuttles ADH from the posterior pituitary to its destinations, reinforcing key concepts in a fun, interactive format. Think you have what it takes? Take the challenge now, then explore SIADH and DI for an extra brain workout or dive into our full endocrine system quiz to see how you score!

Where in the brain is antidiuretic hormone (ADH) primarily synthesized?
Supraoptic nucleus of the hypothalamus
Anterior pituitary
Posterior pituitary
Adrenal medulla
ADH is synthesized in the magnocellular neurons of the supraoptic nucleus and paraventricular nucleus of the hypothalamus, with the supraoptic nucleus being the primary site. After synthesis, it is packaged and transported down the axons to the posterior pituitary for storage and release. This central origin is critical for integrating osmotic and volume signals. Source
Where is ADH stored before release into the bloodstream?
Hypothalamus
Anterior pituitary
Posterior pituitary
Thyroid gland
After synthesis in the hypothalamus, ADH is transported along the hypothalamic - hypophyseal tract and stored in the nerve terminals of the posterior pituitary (neurohypophysis). It is released into the bloodstream when neurosecretory signals trigger exocytosis of those terminals. The anterior pituitary does not store ADH. Source
What is the primary physiological trigger for ADH release?
Reduced skin temperature
Decreased blood glucose
Increased plasma osmolarity
Elevated blood calcium
The main stimulus for ADH release is an increase in plasma osmolarity detected by hypothalamic osmoreceptors. Even small increases in osmolarity above the set point prompt ADH secretion to conserve water. Changes in glucose or calcium do not directly regulate ADH release. Source
What is the principal action of ADH on the kidneys?
Block urea transport
Increase water reabsorption in collecting ducts
Inhibit Na+/K+ ATPase
Stimulate renin release
ADH increases the permeability of the renal collecting ducts to water by promoting insertion of aquaporin-2 channels in the apical membrane. This action concentrates the urine and minimizes water loss. It does not directly inhibit Na+/K+ ATPase or control renin release. Source
Which receptor subtype does ADH bind to in the kidney to exert its antidiuretic effect?
V3 receptor
V1 receptor
V2 receptor
Beta-2 adrenergic receptor
In the kidney, ADH binds to V2 receptors on the basolateral membrane of principal cells in the collecting duct. This receptor activates a Gs protein and increases cAMP, leading to aquaporin-2 insertion. V1 receptors are primarily on vascular smooth muscle. Source
Which second messenger is primarily activated by ADH binding to its V2 receptor in the kidney?
cAMP
IP3/DAG
Ca2+ influx
cGMP
ADH binding to the V2 receptor activates a Gs protein which stimulates adenylate cyclase, increasing intracellular cAMP. This rise in cAMP activates PKA and leads to aquaporin-2 trafficking. IP3/DAG is linked to V1 receptor activation, not V2. Source
Which water channel protein is inserted into the collecting duct membrane in response to ADH?
AQP1
AQP4
AQP3
AQP2
Aquaporin-2 (AQP2) is the principal water channel that translocates to the apical membrane of collecting duct principal cells in response to ADH stimulation. AQP1 is found in proximal tubules and descending limb of Henle, while AQP3 and AQP4 are on the basolateral side. Source
What effect does ADH have on urine volume and osmolality?
Increased volume, increased osmolality
No change in volume or osmolality
Increased volume, decreased osmolality
Decreased volume, increased osmolality
By promoting water reabsorption in the collecting ducts, ADH reduces urine volume and raises urine osmolality. This conserves body water during dehydration. Without ADH, large volumes of dilute urine are produced. Source
Which receptors detect blood pressure changes that can trigger ADH release?
Baroreceptors in the carotid sinus
Proprioceptors in muscles
Osmoreceptors in the hypothalamus
Chemoreceptors in the medulla
Low blood pressure is sensed by baroreceptors located in the carotid sinus and aortic arch. A decrease in stretch triggers ADH release to conserve water and raise vascular tone indirectly. Hypothalamic osmoreceptors respond to osmolarity, not pressure. Source
Through which neuronal tract is ADH transported from the hypothalamus to the posterior pituitary?
Corticospinal tract
Spinothalamic tract
Pyramidal tract
Hypothalamic - hypophyseal tract
ADH is transported along the hypothalamic - hypophyseal tract through axonal transport from the magnocellular neurons in the hypothalamus to the posterior pituitary. This specialized neurovascular structure enables rapid hormone release into circulation. Other tracts carry motor or sensory signals, not hormones. Source
What is the approximate half-life of ADH in the bloodstream?
15 - 20 minutes
1 - 2 hours
1 - 2 minutes
6 - 8 hours
The circulating half-life of ADH is around 15 - 20 minutes. It is rapidly cleared by hepatic and renal metabolism. This relatively short half-life allows for quick adjustments in water balance. Source
Which class of hormone does ADH belong to?
Steroid hormone
Peptide hormone
Amino acid derivative
Eicosanoid
ADH is a nonapeptide hormone composed of nine amino acids. It is synthesized as a larger preprohormone and processed to yield the active peptide. Steroid hormones are lipid-based, whereas eicosanoids derive from fatty acids. Source
Besides the kidney, which tissue responds directly to ADH?
Pancreatic islets
Thyroid gland
Vascular smooth muscle
Adrenal cortex
ADH binds to V1 receptors on vascular smooth muscle cells, causing vasoconstriction and helping to raise blood pressure. The kidney's V2 receptors mediate water reabsorption. Other endocrine glands are not direct targets. Source
Which G protein subunit is activated by ADH at V1 receptors?
Gq
Gs
G12/13
Gi
ADH binding to the V1 receptor activates the Gq protein, which then stimulates phospholipase C to produce IP3 and DAG, leading to increased intracellular calcium and vasoconstriction. Gs is linked with V2 receptors. Source
Which electrolyte disturbance is characteristic of the syndrome of inappropriate ADH secretion (SIADH)?
Hypernatremia
Hyponatremia
Hypokalemia
Hypercalcemia
In SIADH, excessive ADH causes water retention leading to dilutional hyponatremia. Plasma sodium concentration falls while total body sodium is normal or slightly increased. Other electrolytes are less affected. Source
A deficiency in ADH secretion leads to which condition?
Addison's disease
Nephrotic syndrome
Cushing's syndrome
Central diabetes insipidus
Central diabetes insipidus results from inadequate ADH production or release by the hypothalamus or posterior pituitary, causing polyuria and polydipsia. Nephrogenic DI arises from renal insensitivity to ADH. Other listed diseases involve different hormones. Source
What components constitute the preprohormone of ADH as initially synthesized in the hypothalamus?
Prolactin, ADH, oxytocin
Signal peptide, ADH, albumin
Signal peptide, ADH, neurophysin II
Oxytocin, ADH, thyroxine
ADH is synthesized as part of a larger preprohormone that includes an N-terminal signal peptide, the active ADH nonapeptide, and a carrier protein called neurophysin II. Proteolytic processing removes the signal peptide and separates neurophysin II from mature ADH. This arrangement assists proper folding and transport. Source
Which circumventricular organ contains the primary osmoreceptors that regulate ADH secretion?
Pineal gland
Organum vasculosum of the lamina terminalis (OVLT)
Area postrema
Subfornical organ
The organum vasculosum of the lamina terminalis (OVLT) is the main circumventricular organ housing osmosensitive neurons that detect plasma osmolarity changes and signal the hypothalamus to modulate ADH release. The subfornical organ also senses angiotensin II but OVLT is the primary osmoregulatory site. Source
Which cellular target does PKA phosphorylate to promote water channel insertion in response to ADH?
Aquaporin-2 - containing vesicles
Na+/K+ ATPase pumps
Glucocorticoid receptors
UT-A1 urea transporters
Upon ADH binding to V2 receptors, cAMP activates PKA which phosphorylates proteins on aquaporin-2 - containing vesicles, promoting their fusion with the apical membrane of collecting duct cells. This process increases water permeability. Other listed targets are not directly phosphorylated in this pathway. Source
ADH enhances urea recycling in the inner medullary collecting duct by upregulating which transporter?
SGLT2
UT-A1
NKCC2
NHE3
ADH increases the expression and activity of the UT-A1 urea transporter in the inner medullary collecting duct, facilitating urea reabsorption into the medullary interstitium and contributing to the corticomedullary osmotic gradient. NKCC2, SGLT2, and NHE3 are transporters in other nephron segments. Source
Which diagnostic test differentiates central diabetes insipidus from nephrogenic diabetes insipidus?
Water deprivation test alone
Desmopressin administration
Oral glucose tolerance test
ACTH stimulation test
After a water deprivation test, administration of desmopressin (a synthetic ADH analog) will increase urine osmolality in central DI but not in nephrogenic DI, because the latter has renal insensitivity to ADH. This helps distinguish the two conditions. Source
Mutations in which gene most commonly cause X-linked nephrogenic diabetes insipidus?
AVPR2
NKCC2
V2R
AQP2
X-linked nephrogenic DI is most often due to mutations in the AVPR2 gene encoding the V2 receptor for ADH, leading to renal insensitivity. AQP2 mutations cause autosomal forms. V2R is another name for AVPR2 but not a distinct gene. NKCC2 is involved in loop function. Source
Which cranial nerve carries baroreceptor afferent signals from the carotid sinus to regulate ADH secretion?
Vagus nerve (X)
Glossopharyngeal nerve (IX)
Trigeminal nerve (V)
Facial nerve (VII)
Baroreceptors in the carotid sinus send stretch information via the glossopharyngeal nerve (cranial nerve IX) to the brainstem, influencing ADH release through autonomic pathways. The vagus nerve carries signals from the aortic arch but not the carotid sinus. Source
Where are aquaporin-2 channels inserted in response to ADH binding?
Basement membrane of intercalated cells
Basolateral membrane of principal cells
Apical (luminal) membrane of principal cells
Endothelial cells
ADH induces translocation of aquaporin-2 - containing vesicles to the apical (luminal) membrane of principal cells in the collecting duct, allowing water reabsorption from urine back into cells. The basolateral membrane contains other aquaporins for water exit. Source
Which transcription factor is phosphorylated by PKA to upregulate genes involved in ADH's antidiuretic effects?
CREB
STAT3
NF-?B
SP1
PKA activated by cAMP phosphorylates the transcription factor CREB (cAMP response element - binding protein), which then binds to DNA to enhance transcription of genes such as aquaporin-2 and UT-A1 involved in water and urea transport. This regulatory step sustains the antidiuretic response over time. CREB is a well-characterized mediator of cAMP-dependent gene expression. Source
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Study Outcomes

  1. Understand endocrine system components -

    Participate in our endocrine system quiz to grasp how glands, hormones, and feedback loops interact to maintain physiological balance.

  2. Describe how ADH travels to its target cells via the bloodstream -

    Explain the journey of antidiuretic hormone from the posterior pituitary through blood vessels to its renal receptors, highlighting key transport steps.

  3. Analyze gland interactions in ADH secretion -

    Differentiate the roles of the hypothalamus and posterior pituitary in producing and releasing ADH, using hormone function quiz scenarios to reinforce learning.

  4. Identify feedback loops controlling ADH release -

    Outline negative feedback mechanisms that regulate ADH levels in response to plasma osmolarity changes, tested through endocrine system quiz questions.

  5. Apply knowledge to interpret hormone transport mechanisms -

    Use quiz scenarios to apply concepts of hormone transport mechanisms and predict ADH distribution outcomes in physiological and clinical contexts.

  6. Evaluate clinical implications of ADH transport dysfunction -

    Assess how impairments in ADH transport via the bloodstream can lead to disorders like diabetes insipidus, reinforcing insights from gland functions test.

Cheat Sheet

  1. Neurohypophyseal Synthesis and Release -

    Antidiuretic hormone (ADH) is synthesized in the hypothalamic supraoptic and paraventricular nuclei and then stored in the posterior pituitary until triggered for release. Osmoreceptors detect plasma osmolarity above ~280 mOsm/kg, prompting vesicular exocytosis (Guyton & Hall, 2020). This foundational mechanism is a staple concept in any endocrine system quiz.

  2. Endocrine Transport Mechanism -

    Once released, ADH travels freely dissolved in plasma rather than bound to carrier proteins, allowing rapid distribution within its ∼20-minute half-life (Boron & Boulpaep, 2017). This direct hormone transport mechanism exemplifies classic "endocrine" signaling, circulating from the posterior pituitary to distant targets. Remember "free flow, fast function" to recall its unbound nature.

  3. Receptor Binding and Signal Transduction -

    ADH binds to V₂ receptors on kidney collecting duct cells, activating G_s proteins that elevate cAMP and trigger aquaporin-2 channel insertion (Endocrine Society Guidelines, 2021). The mnemonic "V₂ = Volume control" helps link receptor subtype to water reabsorption. This cascade is a frequent focus of hormone function quizzes.

  4. Aquaporin Channels and Water Reabsorption -

    Inserted aquaporin-2 channels increase water permeability in the collecting duct, concentrating urine and reducing plasma osmolarity (National Institutes of Health). A quick memory aid: "So Pee Less" summarizes ADH's effect. Understanding this allows you to ace questions on hormone transport and action.

  5. Negative Feedback and Clinical Relevance -

    Rising blood volume or decreasing osmolarity inhibits further ADH release via baroreceptors and osmoreceptors, completing a negative feedback loop (Marieb & Hoehn, 2018). In clinical contexts, desmopressin testing and the water deprivation test diagnose diabetes insipidus by evaluating this feedback. Integrating these examples strengthens your gland functions test readiness.

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