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Quizzes > Health & Medicine > Human Anatomy & Medicine

Take the Vasodilation vs Vasoconstriction Quiz and See How You Score!

Discover the Difference Between Vasodilation and Vasoconstriction - Start Quiz!

Difficulty: Moderate
2-5mins
Learning OutcomesCheat Sheet
Paper art illustration of two stylized blood vessels side by side one dilated one constricted on dark blue quiz backdrop

Are you ready to dive into the fascinating world of vasodilation vs vasoconstriction? Our free blood vessels quiz tests your grasp of the vasodilation definition, clarifies the vasoconstriction definition, and explores the difference between vasodilation and vasoconstriction. Discover how vascular tone shifts and how blood vessel response adapts under various conditions. Whether you're a student, a healthcare pro, or simply curious about circulatory mechanics, this quiz sharpens your knowledge and boosts your confidence. Take on the challenge now with our cardiovascular system quiz and see if you can ace every question - your mastery awaits!

What term describes the widening of blood vessels?
Vasodilation
Vasoconstriction
Angiogenesis
Vasculogenesis
Vasodilation is the process by which blood vessels widen due to relaxation of smooth muscle in the vessel wall, reducing vascular resistance and increasing blood flow. It is the opposite of vasoconstriction and plays a key role in regulating blood pressure and tissue perfusion. source
Which condition is characterized by narrowing of blood vessels?
Vasoconstriction
Vasodilation
Hypertension
Hypotension
Vasoconstriction is the narrowing of blood vessels resulting from contraction of vascular smooth muscle, increasing vascular resistance and often raising blood pressure. Hypertension refers to high blood pressure but is not the mechanism itself. source
Which molecule is a potent endogenous vasodilator?
Nitric oxide
Endothelin-1
Angiotensin II
Epinephrine
Nitric oxide is produced by endothelial cells and diffuses into vascular smooth muscle to activate guanylate cyclase, increasing cGMP and causing relaxation. Endothelin-1 and angiotensin II are vasoconstrictors. source
Histamine causes vasodilation primarily by which mechanism?
Relaxing vascular smooth muscle and increasing permeability
Stimulating smooth muscle contraction
Promoting platelet aggregation
Activating the renin–angiotensin system
Histamine binds to H1 receptors on endothelial cells, causing them to contract and increasing vascular permeability. It also stimulates the production of nitric oxide, which relaxes smooth muscle and causes vasodilation. source
Which of the following is a vasoconstrictor?
Angiotensin II
Nitric oxide
Bradykinin
Prostacyclin (PGI2)
Angiotensin II is part of the renin–angiotensin system and causes potent vasoconstriction, increasing blood pressure. Bradykinin and prostacyclin are vasodilators, and nitric oxide is a key endothelium-derived relaxing factor. source
Exposure to cold temperature leads to which response in skin blood vessels?
Vasoconstriction
Vasodilation
No change
Only arteriovenous shunts open
Cold exposure triggers sympathetic activation and the venoarteriolar reflex in skin, causing vasoconstriction to reduce heat loss. This response shunts blood away from the skin surface. source
Vasodilation of arterioles has what effect on tissue blood flow?
Increases blood flow
Decreases blood flow
No effect on flow
Stops flow completely
When arterioles dilate, vascular resistance decreases and perfusion pressure increases, leading to elevated blood flow to the downstream capillary beds. This is a fundamental principle of hemodynamics. source
Systemic vasodilation decreases systemic vascular resistance and leads to a drop in which parameter?
Mean arterial pressure
Blood volume
Heart rate
Blood viscosity
Mean arterial pressure (MAP) is directly proportional to cardiac output and systemic vascular resistance. Vasodilation decreases resistance, thus lowering MAP. Blood volume and viscosity are unrelated to acute changes from arteriolar tone. source
Activation of ?2-adrenergic receptors on vascular smooth muscle results in what effect?
Vasodilation
Vasoconstriction
Increased heart rate
Increased contractility
?2-adrenergic receptors on vascular smooth muscle activate adenylate cyclase, raising cAMP and causing relaxation (vasodilation). ?1 effects are primarily cardiac. source
Which subtype of adrenergic receptor predominantly mediates vasoconstriction in peripheral resistance vessels?
?1 receptor
?1 receptor
?2 receptor
M2 muscarinic receptor
?1-adrenergic receptors on vascular smooth muscle promote IP3-mediated Ca²? release and contraction, causing vasoconstriction. ?2 receptors mediate vasodilation. source
In skeletal muscle during exercise, which local factor primarily mediates metabolic vasodilation?
Increased carbon dioxide and decreased pH
Increased oxygen
Increased ATP
Decreased nitric oxide
Active muscle produces CO? and lactic acid, lowering pH and directly relaxing arterioles. Oxygen consumption also plays a role but CO? and H? are primary metabolic vasodilators. source
Endothelin-1 is a potent vasoconstrictor produced by endothelium. Which receptor subtype mediates its vasoconstrictor effect?
ETA receptor
ETB receptor
?2 receptor
V1 vasopressin receptor
ET_A receptors on vascular smooth muscle mediate endothelin-1’s vasoconstrictive actions. ET_B receptors can clear endothelin-1 and in some beds cause vasodilation. source
Which gas is known to cause cerebral vasodilation by relaxing vascular smooth muscle?
Carbon dioxide
Carbon monoxide
Oxygen
Nitrogen
Elevated arterial CO? lowers pH in brain interstitial fluid, causing cerebral arteriolar dilation to increase blood flow and wash out excess CO?. Oxygen has the opposite effect. source
During septic shock, widespread vasodilation is primarily mediated by which molecule?
Nitric oxide
Angiotensin II
Vasopressin
Endothelin-1
In septic shock, inflammatory cytokines induce inducible nitric oxide synthase (iNOS) in endothelium and macrophages, producing large NO amounts that cause profound vasodilation. source
Local autoregulation of renal blood flow includes a myogenic response. What triggers this mechanism?
Change in vessel wall stretch
Accumulation of metabolites
Neural input
Hormonal signal
The myogenic mechanism responds to changes in arteriolar wall stretch: increased pressure stretches smooth muscle, causing reflex contraction and vasoconstriction; decreased stretch causes dilation. source
Increased shear stress on endothelial cells stimulates release of which vasodilator?
Nitric oxide
Endothelin-1
Thromboxane A2
Angiotensin II
Shear stress from flowing blood activates eNOS in endothelial cells, increasing NO production, which diffuses to smooth muscle and induces vasodilation. Endothelin-1 is a vasoconstrictor. source
Sodium nitroprusside lowers blood pressure mainly through which mechanism?
Direct NO release causing smooth muscle relaxation
Inhibition of ACE
?-adrenergic blockade
Calcium channel blockade
Sodium nitroprusside decomposes to release nitric oxide, which activates guanylate cyclase in vascular smooth muscle, increasing cGMP and causing rapid vasodilation of arteries and veins. source
Rho kinase inhibitors promote vasodilation by affecting which process in smooth muscle?
Decreasing myosin light chain phosphorylation
Increasing intracellular Ca²?
Blocking K? channels
Activating phospholipase C
Rho kinase phosphorylates and inhibits myosin light chain phosphatase, promoting sustained contraction. Inhibitors of Rho kinase restore phosphatase activity, leading to dephosphorylation and relaxation of smooth muscle. source
Cold-induced vasoconstriction in skin arterioles is mediated primarily through which mechanism?
Venoarteriolar reflex
Myogenic response
Reactive hyperemia
Bradykinin release
The venoarteriolar reflex is a local axon reflex: venous distension from cold triggers sympathetic-mediated constriction of nearby arterioles to reduce heat loss. It is distinct from the myogenic response. source
Endothelium-derived hyperpolarizing factor (EDHF) induces vasodilation by which cellular action?
Hyperpolarizing smooth muscle via K? channels
Increasing cGMP levels
Increasing cAMP levels
Blocking Ca²? influx
EDHF causes the opening of calcium-activated K? channels in smooth muscle, leading to hyperpolarization, decreased Ca²? entry, and vasorelaxation. It complements NO and prostacyclin pathways. source
Reactive hyperemia refers to the transient increase in blood flow following ischemia. Which is the main mediator?
Accumulation of vasodilator metabolites
Myogenic constriction
Nitric oxide alone
Endothelin release
During ischemia, metabolites such as adenosine, CO?, and H? accumulate, causing profound vasodilation once flow is restored. NO may contribute but metabolites are primary. source
Which peptide promotes vasoconstriction and sodium retention, contributing to hypertension?
Endothelin-1
Atrial natriuretic peptide
Bradykinin
Nitric oxide
Endothelin-1 released by endothelial cells is a potent vasoconstrictor and stimulates sodium reabsorption in the kidney, raising blood pressure. Atrial natriuretic peptide has opposite effects. source
During acute hemorrhage, baroreceptor unloading triggers which vascular response?
Widespread vasoconstriction via sympathetic activation
Vasodilation
Massive nitric oxide release
Prostacyclin-mediated dilation
A drop in arterial pressure reduces baroreceptor firing, leading to increased sympathetic outflow and widespread arteriolar vasoconstriction to maintain perfusion pressure. NO and prostacyclin are not primary here. source
In vascular smooth muscle cells, activation of the RhoA/Rho kinase pathway enhances vasoconstriction by inhibiting which enzyme?
Myosin light chain phosphatase
Myosin light chain kinase
Na?/K? ATPase
cGMP phosphodiesterase
Rho kinase phosphorylates the myosin-binding subunit of myosin light chain phosphatase (MLCP), inhibiting it and sustaining myosin light chain phosphorylation and contraction. This calcium-sensitization mechanism enhances vasoconstriction. source
The PI3K/Akt pathway in endothelial cells promotes vasodilation by phosphorylating which target?
Endothelial nitric oxide synthase
Soluble guanylate cyclase
Protein kinase C
Cyclooxygenase
Akt phosphorylates eNOS on specific serine residues, increasing its activity and NO production. This pathway links growth factors and shear stress to vasodilatory responses in the endothelium. source
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Study Outcomes

  1. Define vasodilation and vasoconstriction -

    Identify and articulate the core definitions of vasodilation and vasoconstriction, including key characteristics of each blood vessel response.

  2. Explain mechanisms of vascular tone -

    Describe how smooth muscle activity and signaling molecules regulate vascular tone to influence vessel diameter and blood flow.

  3. Compare vasodilation vs vasoconstriction -

    Contrast the physiological triggers, outcomes, and clinical significance of vasodilation and vasoconstriction to highlight the difference between these responses.

  4. Analyze factors affecting blood vessel diameter -

    Examine how variables such as temperature, hormones, and neural input alter vascular tone and modify blood vessel constriction or dilation.

  5. Apply concepts to real”world scenarios -

    Use case”based questions to predict whether vasodilation or vasoconstriction will occur in specific physiological or environmental contexts.

  6. Interpret quiz feedback -

    Utilize instant feedback from the quiz to identify knowledge gaps and reinforce your understanding of vasoconstriction definition and vasodilation definition.

Cheat Sheet

  1. Core Definitions -

    Vasodilation definition refers to the process where blood vessels widen due to smooth muscle relaxation, whereas vasoconstriction definition is the narrowing of vessels from muscle contraction. Remember "D for Dilate = Diameter up, Flow up" to recall that vasodilation increases blood flow. Grasping these opposing actions clarifies any discussion about vascular tone and blood vessel response.

  2. Biochemical Triggers -

    Endothelial cells release nitric oxide (NO) to activate guanylate cyclase, boosting cGMP and causing smooth muscle relaxation; conversely, endothelin promotes vasoconstriction by raising intracellular Ca2+. A simple mnemonic is "NO = Go (dilate), ET = Stop (constrict)." These molecular signals are key to understanding the difference between vasodilation and vasoconstriction at the cellular level.

  3. Poiseuille's Law in Practice -

    According to Poiseuille's law (Q = πΔPr^4/8ηL), small changes in vessel radius have a dramatic effect on blood flow: doubling r increases flow 16-fold. This formula underscores why even slight vasoconstriction can greatly raise resistance and blood pressure. Mastering this equation helps predict how vascular tone alterations affect overall circulation.

  4. Autonomic Regulation -

    The sympathetic nervous system primarily drives vasoconstriction via α₝-adrenergic receptors, while β₂-adrenergic activation by epinephrine induces vasodilation in skeletal muscle. Parasympathetic influences are less direct but can modulate blood vessel response through acetylcholine-mediated NO release. Recognizing these neural pathways reinforces your grasp of systemic control over vascular tone.

  5. Clinical Applications -

    Medications like nitroglycerin exploit vasodilation to relieve angina by boosting NO, whereas drugs like phenylephrine induce vasoconstriction to raise blood pressure in hypotensive patients. Understanding these interventions highlights the practical difference between vasodilation and vasoconstriction in therapy. Real-world examples ensure you can connect theory to patient care scenarios.

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