Vasoconstriction and Vasodilation Quiz
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Questions and Answers

Which of the following correctly describes how vasoconstriction is potentiated through signal transduction pathways?

  • G12/13 proteins stimulate nucleotide exchange to maintain myosin light chain phosphorylation. (correct)
  • FF activation of RhoA leads to the phosphorylation and activation of myosin light chain phosphatase.
  • Activation of Gq proteins decreases Ca2+ release from intracellular stores.
  • Inhibition of adenylyl cyclase increases cAMP production, promoting vasoconstriction.

    • What role does protein kinase C (PKC) play in the signal transduction of vasoconstriction?

  • PKC enhances the production of cyclic guanosine monophosphate.
  • PKC promotes contraction through phosphorylation events. (correct)
  • PKC decreases intracellular calcium levels.
  • PKC inhibits myosin light chain kinase activity.

    • Which of the following substances primarily supports the process of vasodilation through activating soluble guanylyl cyclase?

  • Myosin light chain.
  • Cyclic adenosine monophosphate.
  • Endothelin-1.
  • Nitric oxide. (correct)

    • Which pathway is involved in sustaining smooth muscle contraction beyond transient increases in intracellular Ca2+?

    <p>Inhibition of myosin light chain phosphatase by Rho-kinase.</p> Signup and view all the answers

    What happens to cyclic adenosine monophosphate (cAMP) levels when Gi-coupled receptors are activated?

    <p>cAMP levels decrease, relieving MLCK inhibition.</p> Signup and view all the answers

    Which of the following best describes the overall effect of vasoactive substances on blood vessels?

    <p>They can either increase or decrease blood pressure and/or heart rate.</p> Signup and view all the answers

    Which mechanism is specifically involved in the contraction of vascular smooth muscle through MLCK activation?

    <p>Reduced levels of cyclic AMP.</p> Signup and view all the answers

    What is the primary function of nitric oxide in the vascular endothelium?

    <p>Relax smooth muscles by increasing cGMP formation</p> Signup and view all the answers

    Which mechanism contributes to the relaxation of smooth muscle cells by nitric oxide?

    <p>Activation of calcium-dependent K+ channels</p> Signup and view all the answers

    What role does prostacyclin (PGI2) play in the vascular system?

    <p>Acts on Gs-coupled receptors to promote vasodilation</p> Signup and view all the answers

    What is a significant risk associated with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in patients with hypertension?

    <p>Reduced prostacyclin production</p> Signup and view all the answers

    What type of molecules are endothelins, and what is their primary action?

    <p>Potent vasoconstrictors produced in endothelial cells</p> Signup and view all the answers

    Which endothelin isoform is primarily involved in cardiovascular actions?

    <p>ET-1</p> Signup and view all the answers

    What physiological effect is associated with endothelin when released from endothelial cells?

    <p>Promotion of muscle contraction</p> Signup and view all the answers

    What triggers the production of nitric oxide in endothelial cells?

    <p>Histamine, acetylcholine, or bradykinin stimulation</p> Signup and view all the answers

    How does the vascular endothelium primarily influence cardiovascular health?

    <p>By releasing vasoactive mediators</p> Signup and view all the answers

    What is a common effect that occurs when using losartan or valsartan to block angiotensin's effects?

    <p>Compensatory increase in renin and angiotensin I</p> Signup and view all the answers

    Which statement accurately describes the action of bradykinin?

    <p>It induces bronchoconstriction and cough.</p> Signup and view all the answers

    What is the function of natriuretic peptides like ANP and BNP in the renal system?

    <p>Inhibition of renin and aldosterone secretion</p> Signup and view all the answers

    Which of the following is a notable characteristic of aliskiren compared to losartan and valsartan?

    <p>It is a renin inhibitor.</p> Signup and view all the answers

    What potential adverse effect is associated with the use of ACE inhibitors?

    <p>Accumulation of bradykinin</p> Signup and view all the answers

    What is the effect of ET-1 binding to ETB receptors on endothelial cells?

    <p>Activation of eNOS and COX leading to NO release</p> Signup and view all the answers

    Which mechanism is indicated as a negative feedback loop in the context of vascular tone regulation?

    <p>Activation of α2-adrenergic autoreceptors inhibiting norepinephrine release</p> Signup and view all the answers

    How do endothelins compare to norepinephrine in terms of potency as vasoconstrictors?

    <p>They are significantly more potent than norepinephrine</p> Signup and view all the answers

    What role do β2-adrenergic receptors play in vascular smooth muscle cells?

    <p>Mediating relaxation of smooth muscle through Gs pathways</p> Signup and view all the answers

    In which pathophysiological condition are endothelins suggested to play a role?

    <p>Pulmonary hypertension</p> Signup and view all the answers

    What effect does sympathetic nervous system activation have on vascular smooth muscle?

    <p>It releases norepinephrine leading to smooth muscle contraction</p> Signup and view all the answers

    Which of the following compounds inhibits the release of ET-1?

    <p>Prostacyclin</p> Signup and view all the answers

    What is the primary action of bosentan in clinical settings?

    <p>Antagonizing endothelin receptors</p> Signup and view all the answers

    What effect does the release of epinephrine have on vascular smooth muscle via β2 receptors?

    <p>Relaxation through Gs signaling pathways</p> Signup and view all the answers

    Which vascular effect is primarily mediated by ETA receptors on smooth muscle cells?

    <p>Vasoconstriction through increased IP3 and DAG</p> Signup and view all the answers

    What primarily influences the effects of epinephrine on vascular beds?

    <p>The dose of epinephrine and receptor composition</p> Signup and view all the answers

    Which receptor does epinephrine have a higher affinity for at lower concentrations?

    <p>β2 receptors</p> Signup and view all the answers

    During a 'fight or flight' response, blood flow is primarily diverted from which area?

    <p>Skin and viscera</p> Signup and view all the answers

    What is the role of M3-muscarinic receptors in vascular function?

    <p>Mediate vasodilation via NO release</p> Signup and view all the answers

    Which humoral mediator is produced from circulating angiotensinogen?

    <p>Angiotensin I</p> Signup and view all the answers

    What effect does angiotensin II primarily have on blood vessels?

    <p>Constricts arterioles</p> Signup and view all the answers

    What type of medication is captopril classified as?

    <p>ACE inhibitor</p> Signup and view all the answers

    What is the primary action of bradykinin in the vascular system?

    <p>Promote vasodilation</p> Signup and view all the answers

    What common condition is associated with increased angiotensin II levels?

    <p>Hypertension</p> Signup and view all the answers

    Which hormone is responsible for increasing aldosterone secretion?

    <p>Angiotensin II</p> Signup and view all the answers

    Study Notes

    Pharmacology of Vasoactive Substances

    • Vasoactive substances are endogenous or pharmaceutical drugs impacting blood vessel smooth muscles.
    • These substances include vasoconstrictors, vasodilators, and mixed-effect agents.
    • Antagonists or enzymes producing these substances have clinical uses.
    • Vasoactive substances affect blood pressure and heart rate via vascular activity.

    Vasoconstriction Signal Transduction Pathway

    • First, Gq protein-coupled receptors (GPCRs) activate phospholipase C (PLC), producing inositol triphosphate (IP3) and diacylglycerol (DAG).
    • IP3 releases calcium from intracellular stores.
    • DAG activates protein kinase C, promoting contraction via phosphorylation.
    • Second, G12/13 proteins stimulate RhoA, activating Rho-kinase for maintaining myosin light chain (MLC) phosphorylation.
    • Third, Gi-coupled receptors inhibit adenylyl cyclase, reducing cyclic adenosine monophosphate (cAMP). This reduces protein kinase A (PKA) activity, relieving the inhibition of myosin light chain kinase (MLCK).

    Vasodilation Signal Transduction Pathway

    • Vasodilation is potentiated by two pathways.
    • First, Gs-coupled receptors stimulate cAMP formation, PKA activation, MLCK inhibition, and ATP-regulated K+ channel opening.
    • Second, nitric oxide (NO) activates soluble guanylyl cyclase (sGC) to produce cyclic guanosine monophosphate (cGMP).
    • cGMP-dependent protein kinase phosphorylates downstream targets, relaxing smooth muscle.

    Regulators of Vascular Smooth Muscle Tone

    • Four key regulators: vascular endothelium, autonomic nervous system, humoral regulators, local environmental factors.

    Vascular Endothelium

    • Endothelial cells release vasoactive mediators:
      • Prostacyclin (PGI2) and nitric oxide (NO) (vasodilators)
      • Endothelin (vasoconstrictor).
    • Nitric oxide (NO): relaxes smooth muscles by increasing cGMP production, stimulated by acetylcholine, histamine, or bradykinin. Directly activates Ca2+-dependent K+ channels.
    • Prostacyclin (PGI2): a vasodilator produced from arachidonic acid via cyclooxygenase (COX) enzymes. Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit COX enzymes, affecting prostacyclin production, and needs caution in hypertensive patients.
    • Endothelin: a potent and long-acting vasoconstricting peptide formed in endothelial cells. Three peptides (ET-1, ET-2, ET-3) are identified; ET-1 is predominant and participates in cardiovascular actions. Its release is influenced (inhibited) by several factors, including prostacyclin, nitric oxide, and atrial natriuretic peptide.

    Autonomic Nervous System

    • The sympathetic nervous system plays a crucial role in determining vascular tone by releasing norepinephrine from nerve terminals.
    • Norepinephrine binds to alpha-adrenergic receptors (alpha 1 and alpha 2), leading to smooth muscle contraction. Presynaptic alpha 2 autoreceptors help to inhibit further norepinephrine release (negative feedback).
    • Epinephrine, released from the adrenal medulla during sympathetic activation, activates both alpha and beta-2 adrenergic receptors on vascular smooth muscle. Beta-2 receptors lead to smooth muscle relaxation.

    Humoral Regulators

    • Various humoral mediators contribute to vascular tone regulation in addition to the autonomic nervous system:
      • Circulating catecholamines (e.g., epinephrine)
      • Angiotensin II
      • Natriuretic peptides
      • Bradykinin
      • Calcitonin gene-related peptide (CGRP)
      • Antidiuretic hormone/arginine vasopressin
      • Neuropeptide Y
      • Substance P, neurokinins
      • Vasoactive intestinal peptide (VIP)

    Angiotensin and Angiotensin Antagonists

    • Angiotensin I, an inactive decapeptide, is formed from angiotensinogen by renin, released from the juxtaglomerular apparatus.
    • ACE (angiotensin-converting enzyme) converts angiotensin I to the active octapeptide, angiotensin II.
    • Angiotensin II increases in conditions of decreased blood volume; it's found elevated in patients with hypertension treated with diuretics.
    • Angiotensin II acts through angiotensin II receptor subtype 1 (AT1) G protein-coupled receptors stimulating intracellular pathways, leading to increased blood pressure.
    • Angiotensin II leads to increased aldosterone secretion and intravascular volume increase.
    • Angiotensin II is degraded by peptidases (angiotensinases).
    • Angiotensin II receptor blockers (ARBs) and ACE inhibitors can block the effects of angiotensin II. - ACE inhibitors decrease angiotensin II formation. - ARBs block the angiotensin II receptor.

    Other Vasodilators

    • K+ channel openers: directly cause arterial vasodilation by opening K+ATP channels, leading to membrane hyperpolarization.
    • Nitric oxide (NO) donors: organic nitrates and nitroprusside release NO, leading to smooth muscle relaxation.
    • Phosphodiesterase type 5 (PDE5) inhibitors: increase cGMP levels, promoting vascular smooth muscle relaxation (e.g., sildenafil).
    • Other agents such as the alpha 1-adrenergic antagonists and nesiritide are also mentioned.

    Clinical Uses of Vasoactive Drugs

    • Vasoactive drugs are used in various conditions, including systemic hypertension, heart failure, shock, peripheral vascular disease, and pulmonary hypertension. Some agents used to treat pulmonary hypertension are endothelin receptor antagonists.

    Ca2+ Channel Blockers

    • Ca2+ channel blockers are commonly prescribed to manage hypertension and angina, primarily acting as arterial vasodilators.
    • Ca2+ channel blockers bind to both vascular smooth muscle and cardiac myocytes as positive-lusitropic and cardiac agents.

    K+ Channel Openers

    • K+ channel openers directly vasodilate arteries by opening K+ATP channels, hyperpolarizing cells to prevent Ca2+ channel opening.
    • The adverse effects of K+ channel openers may include headache, flushing, peripheral edema and increased myocardial oxygen demand.

    Nitric Oxide Donors

    • Organic nitrates and nitroprusside release nitric oxide (NO) causing vasodilation. Sodium nitroprusside releases NO directly.

    Other Vasodilators

    • Other agents such as ACE inhibitors/antagonists, endothelin receptor antagonists, alpha 1-adrenergic antagonists and nesiritide are also discussed as vasodilators.

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    Pharmacology of Vasoactive Substances PDF

    Description

    Test your knowledge on the mechanisms of vasoconstriction and vasodilation, including the roles of key signaling proteins like PKC and nitric oxide. Explore how various substances affect blood vessel behavior and learn about intracellular signaling pathways involved in smooth muscle contraction. This quiz will challenge your understanding of cardiovascular physiology.

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